Journal Description
Antioxidants
Antioxidants
is an international, peer-reviewed, open access journal, published monthly online by MDPI. The International Coenzyme Q10 Association (ICQ10A), Israel Society for Oxygen and Free Radical Research (ISOFRR) and European Academy for Molecular Hydrogen Research (EAMHR) are affiliated with Antioxidants and their members receive discounts on the article processing charge.
- Open Access— free for readers, with article processing charges (APC) paid by authors or their institutions.
- High Visibility: indexed within Scopus, SCIE (Web of Science), PubMed, PMC, FSTA, PubAg, CAPlus / SciFinder, and other databases.
- Journal Rank: JCR - Q1 (Food Science & Technology) / CiteScore - Q1 (Food Science)
- Rapid Publication: manuscripts are peer-reviewed and a first decision is provided to authors approximately 13.9 days after submission; acceptance to publication is undertaken in 2.6 days (median values for papers published in this journal in the second half of 2023).
- Recognition of Reviewers: reviewers who provide timely, thorough peer-review reports receive vouchers entitling them to a discount on the APC of their next publication in any MDPI journal, in appreciation of the work done.
- Testimonials: See what our editors and authors say about Antioxidants.
- Companion journal: Oxygen.
Impact Factor:
7.0 (2022);
5-Year Impact Factor:
7.3 (2022)
Latest Articles
Perfusion Techniques in Kidney Allograft Preservation to Reduce Ischemic Reperfusion Injury: A Systematic Review and Meta-Analysis
Antioxidants 2024, 13(6), 642; https://doi.org/10.3390/antiox13060642 - 24 May 2024
Abstract
The limited supply and rising demand for kidney transplantation has led to the use of allografts more susceptible to ischemic reperfusion injury (IRI) and oxidative stress to expand the donor pool. Organ preservation and procurement techniques, such as machine perfusion (MP) and normothermic
[...] Read more.
The limited supply and rising demand for kidney transplantation has led to the use of allografts more susceptible to ischemic reperfusion injury (IRI) and oxidative stress to expand the donor pool. Organ preservation and procurement techniques, such as machine perfusion (MP) and normothermic regional perfusion (NRP), have been developed to preserve allograft function, though their long-term outcomes have been more challenging to investigate. We performed a systematic review and meta-analysis to examine the benefits of MP and NRP compared to traditional preservation techniques. PubMed (MEDLINE), Embase, Cochrane, and Scopus databases were queried, and of 13,794 articles identified, 54 manuscripts were included (n = 41 MP; n = 13 NRP). MP decreased the rates of 12-month graft failure (OR 0.67; 95%CI 0.55, 0.80) and other perioperative outcomes such as delayed graft function (OR 0.65; 95%CI 0.54, 0.79), primary nonfunction (OR 0.63; 95%CI 0.44, 0.90), and hospital length of stay (15.5 days vs. 18.4 days) compared to static cold storage. NRP reduced the rates of acute rejection (OR 0.48; 95%CI 0.35, 0.67) compared to in situ perfusion. Overall, MP and NRP are effective techniques to mitigate IRI and play an important role in safely expanding the donor pool to satisfy the increasing demands of kidney transplantation.
Full article
(This article belongs to the Special Issue New Strategies in Preventing Inflammatory and/or Oxidative-Stress-Induced Damages in Ischemia–Reperfusion Injury)
Open AccessArticle
Proteome Analysis Related to Unsaturated Fatty Acid Synthesis by Interfering with Bovine Adipocyte ACSL1 Gene
by
Yanbin Bai, Jingsheng Li, Yali Wei, Zongchang Chen, Zhanxin Liu, Dashan Guo, Xue Jia, Yanmei Niu, Bingang Shi, Xiaolan Zhang, Zhidong Zhao, Jiang Hu, Xiangmin Han, Jiqing Wang, Xiu Liu and Shaobin Li
Antioxidants 2024, 13(6), 641; https://doi.org/10.3390/antiox13060641 - 24 May 2024
Abstract
Unsaturated fatty acids (UFAs) in beef play a vital role in promoting human health. Long-chain fatty acyl-CoA synthase 1 (ACSL1) is a crucial gene for UFA synthesis in bovine adipocytes. To investigate the protein expression profile during UFA synthesis, we performed a proteomic
[...] Read more.
Unsaturated fatty acids (UFAs) in beef play a vital role in promoting human health. Long-chain fatty acyl-CoA synthase 1 (ACSL1) is a crucial gene for UFA synthesis in bovine adipocytes. To investigate the protein expression profile during UFA synthesis, we performed a proteomic analysis of bovine adipocytes by RNA interference and non-interference with ACSL1 using label-free techniques. A total of 3558 proteins were identified in both the NC and si-treated groups, of which 1428 were differentially expressed proteins (DEPs; fold change ≥ 1.2 or ≤ 0.83 and p-value < 0.05). The enrichment analysis of the DEPs revealed signaling pathways related to UFA synthesis or metabolism, including cAMP, oxytocin, fatty acid degradation, glycerol metabolism, insulin, and the regulation of lipolysis in adipocytes (p-value < 0.05). Furthermore, based on the enrichment analysis of the DEPs, we screened 50 DEPs that potentially influence the synthesis of UFAs and constructed an interaction network. Moreover, by integrating our previously published transcriptome data, this study established a regulatory network involving differentially expressed long non-coding RNAs (DELs), highlighting 21 DEPs and 13 DELs as key genes involved in UFA synthesis. These findings present potential candidate genes for further investigation into the molecular mechanisms underlying UFA synthesis in bovines, thereby offering insights to enhance the quality of beef and contribute to consumer health in future studies.
Full article
(This article belongs to the Special Issue Lipid Oxidation in Food and Nutrition)
Open AccessArticle
The Oxidative Potential of Airborne Particulate Matter Research Trends, Challenges, and Future Perspectives—Insights from a Bibliometric Analysis and Scoping Review
by
Luis Felipe Sánchez, Loreto Villacura, Francisco Catalán, Richard Toro Araya and Manuel A. Leiva Guzman
Antioxidants 2024, 13(6), 640; https://doi.org/10.3390/antiox13060640 - 24 May 2024
Abstract
This study is a comprehensive analysis of the oxidative potential (OP) of particulate matter (PM) and its environmental and health impacts. The researchers conducted a bibliometric analysis and scoping review, screening 569 articles and selecting 368 for further analysis. The study found that
[...] Read more.
This study is a comprehensive analysis of the oxidative potential (OP) of particulate matter (PM) and its environmental and health impacts. The researchers conducted a bibliometric analysis and scoping review, screening 569 articles and selecting 368 for further analysis. The study found that OP is an emerging field of study, with a notable increase in the number of publications in the 2010s compared to the early 2000s. The research is primarily published in eight journals and is concentrated in a few academic and university-based institutions. The study identified key research hotspots for OP-PM, emphasizing the importance of capacity building, interdisciplinary collaboration, understanding emission sources and atmospheric processes, and the impacts of PM and its OP. The study highlighted the need to consider the effects of climate change on OP-PM and the regulatory framework for PM research. The findings of this study will contribute to a better understanding of PM and its consequences, including human exposure and its effects. It will also inform strategies for managing air quality and protecting public health. Overall, this study provides valuable insights into the field of OP-PM research and highlights the need for continued research and collaboration to address the environmental and health impacts of PM.
Full article
(This article belongs to the Section Health Outcomes of Antioxidants and Oxidative Stress)
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Graphical abstract
Graphical abstract
Full article ">Figure 1
<p>(<b>a</b>) The PRISMA-ScR flow chart used to search for articles in the WoS database. (<b>b</b>) Bibliometric summary metrics of the article collection. (<b>c</b>) Trends of articles published on the oxidative potential of airborne particulate matter.</p> Full article ">Figure 2
<p>(<b>a</b>) Histogram and cartogram of geographical distribution of articles according to country of authors and coauthors, (<b>b</b>) histogram and cartogram of geographical distribution of articles according to country of corresponding author(s), and (<b>c</b>) origin–destination diagram showing collaboration between corresponding authors from one country with respect to others. Names of countries in ISO 3166-1 alpha-3 codes [<a href="#B65-antioxidants-13-00640" class="html-bibr">65</a>].</p> Full article ">Figure 3
<p>(<b>a</b>) Bradford’s law of most prominent sources. (<b>b</b>) Number of published articles (NP) per journal. (<b>c</b>) Total number of local citations (TCs) per journal. (<b>d</b>) Impact factor (IF) of the journal. (<b>e</b>) H-index of journal considering the articles from the collection on OP-PM.</p> Full article ">Figure 4
<p>(<b>a</b>) Frequency distribution of publications using Lotka’s law. (<b>b</b>) Ranking of the most relevant authors according to the number of published articles (NP), (<b>c</b>) number of total local citations (LCs), and (<b>d</b>) H-index. (<b>e</b>) The cooperation networks of the articles produced by the authors.</p> Full article ">Figure 5
<p>(<b>a</b>) Ranking of the most relevant research institutions in the area of OP-MP. (<b>b</b>) Cooperation networks for production by institutions.</p> Full article ">Figure 6
<p>Analysis of hotspots in OP-PM from 2003 to 2021. (<b>a</b>) Co-occurrence network of WoS subject categories. (<b>b</b>) Co-occurrence network of author keywords.</p> Full article ">
Full article ">Figure 1
<p>(<b>a</b>) The PRISMA-ScR flow chart used to search for articles in the WoS database. (<b>b</b>) Bibliometric summary metrics of the article collection. (<b>c</b>) Trends of articles published on the oxidative potential of airborne particulate matter.</p> Full article ">Figure 2
<p>(<b>a</b>) Histogram and cartogram of geographical distribution of articles according to country of authors and coauthors, (<b>b</b>) histogram and cartogram of geographical distribution of articles according to country of corresponding author(s), and (<b>c</b>) origin–destination diagram showing collaboration between corresponding authors from one country with respect to others. Names of countries in ISO 3166-1 alpha-3 codes [<a href="#B65-antioxidants-13-00640" class="html-bibr">65</a>].</p> Full article ">Figure 3
<p>(<b>a</b>) Bradford’s law of most prominent sources. (<b>b</b>) Number of published articles (NP) per journal. (<b>c</b>) Total number of local citations (TCs) per journal. (<b>d</b>) Impact factor (IF) of the journal. (<b>e</b>) H-index of journal considering the articles from the collection on OP-PM.</p> Full article ">Figure 4
<p>(<b>a</b>) Frequency distribution of publications using Lotka’s law. (<b>b</b>) Ranking of the most relevant authors according to the number of published articles (NP), (<b>c</b>) number of total local citations (LCs), and (<b>d</b>) H-index. (<b>e</b>) The cooperation networks of the articles produced by the authors.</p> Full article ">Figure 5
<p>(<b>a</b>) Ranking of the most relevant research institutions in the area of OP-MP. (<b>b</b>) Cooperation networks for production by institutions.</p> Full article ">Figure 6
<p>Analysis of hotspots in OP-PM from 2003 to 2021. (<b>a</b>) Co-occurrence network of WoS subject categories. (<b>b</b>) Co-occurrence network of author keywords.</p> Full article ">
Open AccessArticle
Antioxidative Potential and Ameliorative Effects of Rice Bran Fermented with Lactobacillus against High-Fat Diet-Induced Oxidative Stress in Mice
by
Tingting Yin, Yidan Chen, Wenzhao Li, Tingting Tang, Tong Li, Binbin Xie, Dong Xiao and Hailun He
Antioxidants 2024, 13(6), 639; https://doi.org/10.3390/antiox13060639 - 24 May 2024
Abstract
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Rice bran is an important byproduct of the rice polishing process, rich in nutrients, but it is underutilized and often used as feed or discarded, resulting in a huge amount of waste. In this study, rice bran was fermented by Lactobacillus fermentum MF423
[...] Read more.
Rice bran is an important byproduct of the rice polishing process, rich in nutrients, but it is underutilized and often used as feed or discarded, resulting in a huge amount of waste. In this study, rice bran was fermented by Lactobacillus fermentum MF423 to obtain a product with high antioxidant activity. First, a reliable and efficient method for assessing the antioxidant capacity of the fermentation products was established using high-performance liquid chromatography (HPLC), which ensured the consistency of the batch fermentation. The fermented rice bran product (FLRB) exhibited significant antioxidant activity in cells, C. elegans, and hyperlipidemic mice. Transcriptome analysis of mouse livers showed that the expression of plin5 was upregulated in diabetic mice administered FLRB, thereby preventing the excessive production of free fatty acids (FFAs) and the subsequent generation of large amounts of reactive oxygen species (ROS). These studies lay the foundation for the application of rice bran fermentation products.
Full article
Figure 1
Figure 1
<p>Hydroxyl radical scavenging activity was assessed in the products of fermented rice bran by different <span class="html-italic">Lactobacillus</span> strains at various fermentation times. <span class="html-italic">Lactobacillus plantarum</span> (<b>a</b>); <span class="html-italic">Lactobacillus fermentum</span> (<b>b</b>); <span class="html-italic">Lactobacillus casei</span> (<b>c</b>); “<sup>#</sup>” represents the comparison with the unfermented group, “*”, “**”, and “***” represents <span class="html-italic">p</span> < 0.05, <span class="html-italic">p</span> < 0.01, and <span class="html-italic">p</span> < 0.001.</p> Full article ">Figure 2
<p>Protective effects of MF423 fermented rice bran products against cellular oxidative stress. Intracellular ROS on HUVECs (<b>a</b>), HaCaT (<b>c</b>), HDFs (<b>e</b>) cells indicated as green DCFH-DA fluorescence. Images were taken using fluorescence microscope (magnification, 10×). Statistical analysis was performed to quantify relative fluorescence density of HUVEC (<b>b</b>), HaCaT (<b>d</b>), HDF (<b>f</b>) cells. “<sup>#</sup>” means <span class="html-italic">p</span> < 0.01 compared with control; “**”, and “***” representing <span class="html-italic">p</span> < 0.01, and <span class="html-italic">p</span> < 0.001. compared with model.</p> Full article ">Figure 3
<p>The effect of FLRB on SOD, GSH-Px, and CAT enzyme activity in cells. HUVECs (<b>a</b>–<b>c</b>); HDFs (<b>d</b>–<b>f</b>); HaCaT (<b>g</b>–<b>i</b>). “<sup>#</sup>” means <span class="html-italic">p</span> < 0.01 compared with control; “*”, “**”, and “***” representing <span class="html-italic">p</span> < 0.05, <span class="html-italic">p</span> < 0.01, and <span class="html-italic">p</span> < 0.001 compared with model.</p> Full article ">Figure 4
<p>The protective effects of the fermentation product of MF423 on oxidative stress in <span class="html-italic">C. elegans</span>. (<b>a</b>) The effect of fermented rice bran product (FLRB) on the lifespan of <span class="html-italic">C. elegans</span> (n = 50 worms). (<b>b</b>,<b>c</b>) Effects of FLRB on the antioxidant stress response in <span class="html-italic">C. elegans</span> (n = 50 worms); H<sub>2</sub>O<sub>2</sub>-induced oxidative stress model (<b>b</b>). (<b>c</b>) Methyl viologen-induced oxidative stress model. (<b>d</b>–<b>f</b>) The scavenging effect of FLRB on reactive oxygen species (ROS) in <span class="html-italic">C. elegans</span> (n = 3 groups). Fluorescent images of ROS in worms (100× magnification) (<b>d</b>). Comparison of average fluorescence intensity (<b>e</b>). Comparison of fluorescence accumulation (<b>f</b>). (<b>g</b>–<b>j</b>) The malondialdehyde (MDA) content and antioxidant enzyme activity in <span class="html-italic">C. elegans</span>. MDA (<b>g</b>); glutathione peroxidase (GSH-Px) enzyme activity (<b>h</b>); superoxide dismutase (SOD) enzyme activity (<b>i</b>); catalase (CAT) enzyme activity (<b>j</b>). “*”, “**”, and “***” representing <span class="html-italic">p</span> < 0.05, <span class="html-italic">p</span> < 0.01, and <span class="html-italic">p</span> < 0.001.</p> Full article ">Figure 5
<p>Kyoto Encyclopedia of Genes and Genomes (KEGG) signaling pathway enrichment analysis.</p> Full article ">Figure 6
<p>The expression level of antioxidant genes (n = 6): <span class="html-italic">plin5</span> (<b>a</b>); <span class="html-italic">nrf2</span> (<b>b</b>); <span class="html-italic">ho1</span> (<b>c</b>); <span class="html-italic">gclc</span> (<b>d</b>); <span class="html-italic">nqo1</span> (<b>e</b>); <span class="html-italic">sod2</span> (<b>f</b>). “*”, “**”, and “***” representing <span class="html-italic">p</span> < 0.05, <span class="html-italic">p</span> < 0.01, and <span class="html-italic">p</span> < 0.001.</p> Full article ">Figure 7
<p>Mechanisms of antioxidant action of fermentation products in vivo, red arrows are up, purple arrows are down.</p> Full article ">
<p>Hydroxyl radical scavenging activity was assessed in the products of fermented rice bran by different <span class="html-italic">Lactobacillus</span> strains at various fermentation times. <span class="html-italic">Lactobacillus plantarum</span> (<b>a</b>); <span class="html-italic">Lactobacillus fermentum</span> (<b>b</b>); <span class="html-italic">Lactobacillus casei</span> (<b>c</b>); “<sup>#</sup>” represents the comparison with the unfermented group, “*”, “**”, and “***” represents <span class="html-italic">p</span> < 0.05, <span class="html-italic">p</span> < 0.01, and <span class="html-italic">p</span> < 0.001.</p> Full article ">Figure 2
<p>Protective effects of MF423 fermented rice bran products against cellular oxidative stress. Intracellular ROS on HUVECs (<b>a</b>), HaCaT (<b>c</b>), HDFs (<b>e</b>) cells indicated as green DCFH-DA fluorescence. Images were taken using fluorescence microscope (magnification, 10×). Statistical analysis was performed to quantify relative fluorescence density of HUVEC (<b>b</b>), HaCaT (<b>d</b>), HDF (<b>f</b>) cells. “<sup>#</sup>” means <span class="html-italic">p</span> < 0.01 compared with control; “**”, and “***” representing <span class="html-italic">p</span> < 0.01, and <span class="html-italic">p</span> < 0.001. compared with model.</p> Full article ">Figure 3
<p>The effect of FLRB on SOD, GSH-Px, and CAT enzyme activity in cells. HUVECs (<b>a</b>–<b>c</b>); HDFs (<b>d</b>–<b>f</b>); HaCaT (<b>g</b>–<b>i</b>). “<sup>#</sup>” means <span class="html-italic">p</span> < 0.01 compared with control; “*”, “**”, and “***” representing <span class="html-italic">p</span> < 0.05, <span class="html-italic">p</span> < 0.01, and <span class="html-italic">p</span> < 0.001 compared with model.</p> Full article ">Figure 4
<p>The protective effects of the fermentation product of MF423 on oxidative stress in <span class="html-italic">C. elegans</span>. (<b>a</b>) The effect of fermented rice bran product (FLRB) on the lifespan of <span class="html-italic">C. elegans</span> (n = 50 worms). (<b>b</b>,<b>c</b>) Effects of FLRB on the antioxidant stress response in <span class="html-italic">C. elegans</span> (n = 50 worms); H<sub>2</sub>O<sub>2</sub>-induced oxidative stress model (<b>b</b>). (<b>c</b>) Methyl viologen-induced oxidative stress model. (<b>d</b>–<b>f</b>) The scavenging effect of FLRB on reactive oxygen species (ROS) in <span class="html-italic">C. elegans</span> (n = 3 groups). Fluorescent images of ROS in worms (100× magnification) (<b>d</b>). Comparison of average fluorescence intensity (<b>e</b>). Comparison of fluorescence accumulation (<b>f</b>). (<b>g</b>–<b>j</b>) The malondialdehyde (MDA) content and antioxidant enzyme activity in <span class="html-italic">C. elegans</span>. MDA (<b>g</b>); glutathione peroxidase (GSH-Px) enzyme activity (<b>h</b>); superoxide dismutase (SOD) enzyme activity (<b>i</b>); catalase (CAT) enzyme activity (<b>j</b>). “*”, “**”, and “***” representing <span class="html-italic">p</span> < 0.05, <span class="html-italic">p</span> < 0.01, and <span class="html-italic">p</span> < 0.001.</p> Full article ">Figure 5
<p>Kyoto Encyclopedia of Genes and Genomes (KEGG) signaling pathway enrichment analysis.</p> Full article ">Figure 6
<p>The expression level of antioxidant genes (n = 6): <span class="html-italic">plin5</span> (<b>a</b>); <span class="html-italic">nrf2</span> (<b>b</b>); <span class="html-italic">ho1</span> (<b>c</b>); <span class="html-italic">gclc</span> (<b>d</b>); <span class="html-italic">nqo1</span> (<b>e</b>); <span class="html-italic">sod2</span> (<b>f</b>). “*”, “**”, and “***” representing <span class="html-italic">p</span> < 0.05, <span class="html-italic">p</span> < 0.01, and <span class="html-italic">p</span> < 0.001.</p> Full article ">Figure 7
<p>Mechanisms of antioxidant action of fermentation products in vivo, red arrows are up, purple arrows are down.</p> Full article ">
Open AccessArticle
Dietary Supplementation with Naringin Improves Systemic Metabolic Status and Alleviates Oxidative Stress in Transition Cows via Modulating Adipose Tissue Function: A Lipid Perspective
by
Liuxue Li, Sarula Bai, Huiying Zhao, Jian Tan, Ying Wang, Ao Zhang, Linshu Jiang and Yuchao Zhao
Antioxidants 2024, 13(6), 638; https://doi.org/10.3390/antiox13060638 - 24 May 2024
Abstract
Dairy cows face metabolic challenges around the time of calving, leading to a negative energy balance and various postpartum health issues. Adipose tissue is crucial for cows during this period, as it regulates energy metabolism and supports immune function. Naringin, one of the
[...] Read more.
Dairy cows face metabolic challenges around the time of calving, leading to a negative energy balance and various postpartum health issues. Adipose tissue is crucial for cows during this period, as it regulates energy metabolism and supports immune function. Naringin, one of the main flavonoids in citrus fruit and their byproducts, is a potent antioxidant and anti-inflammatory phytoconstituent. The study aimed to evaluate the effects of supplemental naringin on performance, systemic inflammation, oxidative status, and adipose tissue metabolic status. A total of 36 multiparous Holstein cows (from ~21 d prepartum through 35 d postpartum) were provided a basal control (CON) diet or a CON diet containing naringin (NAR) at 30 g/d per cow. Supplemental NAR increased the yield of raw milk and milk protein, without affecting dry matter intake. Cows fed NAR showed significantly lower levels (p < 0.05) of serum non-esterified fatty acid (NEFA), C-reactive protein, IL-1β, IL-6, malonaldehyde, lipopolysaccharide (LPS), aspartate aminotransferase, and alanine aminotransferase, but increased (p < 0.05) glutathione peroxidase activity relative to those fed CON. Supplemental NAR increased (p < 0.05) adipose tissue adiponectin abundance, decreased inflammatory responses, and reduced oxidative stress. Lipidomic analysis showed that cows fed NAR had lower concentrations of ceramide species (p < 0.05) in the serum and adipose tissue than did the CON-fed cows. Adipose tissue proteomics showed that proteins related to lipolysis, ceramide biosynthesis, inflammation, and heat stress were downregulated (p < 0.05), while those related to glycerophospholipid biosynthesis and the extracellular matrix were upregulated (p < 0.05). Feeding NAR to cows may reduce the accumulation of ceramide by lowering serum levels of NEFA and LPS and increasing adiponectin expression, thereby decreasing inflammation and oxidative stress in adipose tissue, ultimately improving their systemic metabolic status. Including NAR in periparturient cows’ diets improves lactational performance, reduces excessive lipolysis in adipose tissue, and decreases systemic and adipose tissue inflammation and oxidative stress. Integrating lipidomic and proteomic data revealed that reduced ceramide and increased glycerophospholipids may alleviate metabolic dysregulations in adipose tissue, which in turn benefits systemic metabolic status.
Full article
(This article belongs to the Special Issue Natural Antioxidants and Oxidative Stress in Livestock and Poultry)
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Figure 1
<p>Serum and adipose tissue lipidomes. Principal component analysis (PCA) of (<b>a</b>) serum and (<b>b</b>) adipose tissue lipidomics. Orthogonal partial least squares discriminant analysis (OPLS-DA) of (<b>c</b>) serum and (<b>d</b>) adipose tissue lipidomics. Volcano plot of identified lipid species in (<b>e</b>) serum and (<b>f</b>) adipose tissue. Yellow symbols: significantly decreased lipid species (variable importance in projection (VIP) > 1, <span class="html-italic">p</span> < 0.05). Blue symbols: significantly increased lipid species (VIP > 1, <span class="html-italic">p</span> < 0.05). CON, control; NAR; naringin; FC, fold change.</p> Full article ">Figure 2
<p>Lipidomic alteration in serum and adipose tissue samples. Differential lipid species in (<b>a</b>) serum and (<b>b</b>) adipose tissue are presented in the fold-change of NAR relative to CON. KEGG pathway analysis of differential lipid species in (<b>c</b>) serum and (<b>d</b>) adipose tissue samples. BisMePA, bismethyl phosphatidic acid; Cer, ceramide; CL, cardiolipin; Co, coenzyme; DG, diglyceride; Hex2Cer, dihexosylceramide; LPC, lysophosphatidylcholine; MePC, methylphosphatidylcholine; MGDG, monogalactosyldiacylglycerol; OHAFA, (O-acyl)-1-hydroxy fatty acid; PC, phosphatidylcholine; PE, phosphatidylethanolamine; PI, phosphatidylinositol; PIP2, phosphatidylinositol 4,5-bisphosphate; PS, phosphatidylserine; SiE, sitosteryl ester; SM, sphingomyelin; TG, triglyceride; ZyE, zymosteryl.</p> Full article ">Figure 3
<p>Association analysis of the serum and adipose tissue lipidome. (<b>a</b>) The correlation between differential lipid species in the serum and adipose tissue samples by Procrustes analysis; (<b>b</b>) the correlation between differential sphingolipid (SP) species in serum and adipose tissue samples by Procrustes analysis; (<b>c</b>) Pearson’s correlation between serum differential sphingolipids and serum biochemical parameters; (<b>d</b>) Pearson’s correlation between adipose tissue differential sphingolipids and adipose tissue biochemical parameters; (<b>e</b>) Pearson’s correlation between adipose tissue differential glycerophospholipids (top 30 of VIP value) and adipose tissue biochemical parameters. ALT, alanine aminotransferase; ASC, apoptosis-associated speck like protein containing a CARD; AST, aspartate aminotransferase; Cer, ceramide; CL, cardiolipin; CON, control; CRP, C-reactive protein; dMePE, dimethylphosphatidylethanolamine; GSH-Px, glutathione peroxidase; Hex2Cer, dihexosylceramide; IL, interleukin; LPS, lipopolysaccharide; MDA, malonaldehyde; NAR, naringin; NEFA, non-esterified fatty acid; NLRP3, NOD-like receptor thermal protein domain-associated protein 3; PC, phosphatidylcholine; PE, phosphatidylethanolamine; PI, phosphatidylinositol; PS, phosphatidylserine; SM, sphingomyelin; SOD, superoxide dismutase; SP, sphingolipid; TP, total protein.</p> Full article ">Figure 4
<p>Adipose tissue proteome analysis. (<b>a</b>) Venn diagram of the identified proteins; (<b>b</b>) PCA score plots of proteome data; (<b>c</b>) volcano plot of the proteome; (<b>d</b>) heatmap of differentially expressed proteins. CON, control; NAR, naringin; FC, fold change.</p> Full article ">Figure 5
<p>Proteomic alteration in adipose tissue samples. GO enrichment analysis of (<b>a</b>) upregulated differentially expressed proteins (DEP) and (<b>b</b>) downregulated DEP; (<b>c</b>) KEGG enrichment analysis of DEP; (<b>d</b>) selected DEP related to sphingolipid metabolism and glycerophospholipid metabolism; (<b>e</b>) selected DEP related to lipolysis and inflammation; (<b>f</b>) selected DEP related to heat stress and extracellular matrix. * <span class="html-italic">p</span> < 0.05, ** <span class="html-italic">p</span> < 0.01, *** <span class="html-italic">p</span> < 0.001, **** <span class="html-italic">p</span> < 0.0001. CON, control; NAR, naringin.</p> Full article ">Figure 6
<p>Integrated pathway and network analysis of the adipose tissue lipidome and proteome. (<b>a</b>) Diagram of lipid metabolism, including glycerolipid metabolism, glycerophospholipid metabolism, and sphingolipid metabolism; (<b>b</b>) protein–protein interaction (PPI) network of selected differentially expressed proteins (DEP); (<b>c</b>) Pearson’s correlation network between differential lipids (glycerophospholipid and sphingolipid species) and selected DEP; red lines represent positive, while blue lines indicate negative correlations (<span class="html-italic">p</span> < 0.05 and |r| > 0.50); (<b>d</b>) Pearson’s correlation analysis between selected DEP and serum biochemical parameters. * <span class="html-italic">p</span> < 0.05, ** <span class="html-italic">p</span> < 0.01. ALT, alanine aminotransferase; AST, aspartate aminotransferase; Cer, ceramide; CL, cardiolipin; CRP, C-reactive protein; dMePE, dimethylphosphatidylethanolamine; GSH-Px, glutathione peroxidase; IL, interleukin; LPS, lipopolysaccharide; MDA, malonaldehyde; NEFA, non-esterified fatty acid; PC, phosphatidylcholine; PE, phosphatidylethanolamine; PI, phosphatidylinositol; PS, phosphatidylserine; SM, sphingomyelin; SOD, superoxide dismutase; TP, total protein.</p> Full article ">
<p>Serum and adipose tissue lipidomes. Principal component analysis (PCA) of (<b>a</b>) serum and (<b>b</b>) adipose tissue lipidomics. Orthogonal partial least squares discriminant analysis (OPLS-DA) of (<b>c</b>) serum and (<b>d</b>) adipose tissue lipidomics. Volcano plot of identified lipid species in (<b>e</b>) serum and (<b>f</b>) adipose tissue. Yellow symbols: significantly decreased lipid species (variable importance in projection (VIP) > 1, <span class="html-italic">p</span> < 0.05). Blue symbols: significantly increased lipid species (VIP > 1, <span class="html-italic">p</span> < 0.05). CON, control; NAR; naringin; FC, fold change.</p> Full article ">Figure 2
<p>Lipidomic alteration in serum and adipose tissue samples. Differential lipid species in (<b>a</b>) serum and (<b>b</b>) adipose tissue are presented in the fold-change of NAR relative to CON. KEGG pathway analysis of differential lipid species in (<b>c</b>) serum and (<b>d</b>) adipose tissue samples. BisMePA, bismethyl phosphatidic acid; Cer, ceramide; CL, cardiolipin; Co, coenzyme; DG, diglyceride; Hex2Cer, dihexosylceramide; LPC, lysophosphatidylcholine; MePC, methylphosphatidylcholine; MGDG, monogalactosyldiacylglycerol; OHAFA, (O-acyl)-1-hydroxy fatty acid; PC, phosphatidylcholine; PE, phosphatidylethanolamine; PI, phosphatidylinositol; PIP2, phosphatidylinositol 4,5-bisphosphate; PS, phosphatidylserine; SiE, sitosteryl ester; SM, sphingomyelin; TG, triglyceride; ZyE, zymosteryl.</p> Full article ">Figure 3
<p>Association analysis of the serum and adipose tissue lipidome. (<b>a</b>) The correlation between differential lipid species in the serum and adipose tissue samples by Procrustes analysis; (<b>b</b>) the correlation between differential sphingolipid (SP) species in serum and adipose tissue samples by Procrustes analysis; (<b>c</b>) Pearson’s correlation between serum differential sphingolipids and serum biochemical parameters; (<b>d</b>) Pearson’s correlation between adipose tissue differential sphingolipids and adipose tissue biochemical parameters; (<b>e</b>) Pearson’s correlation between adipose tissue differential glycerophospholipids (top 30 of VIP value) and adipose tissue biochemical parameters. ALT, alanine aminotransferase; ASC, apoptosis-associated speck like protein containing a CARD; AST, aspartate aminotransferase; Cer, ceramide; CL, cardiolipin; CON, control; CRP, C-reactive protein; dMePE, dimethylphosphatidylethanolamine; GSH-Px, glutathione peroxidase; Hex2Cer, dihexosylceramide; IL, interleukin; LPS, lipopolysaccharide; MDA, malonaldehyde; NAR, naringin; NEFA, non-esterified fatty acid; NLRP3, NOD-like receptor thermal protein domain-associated protein 3; PC, phosphatidylcholine; PE, phosphatidylethanolamine; PI, phosphatidylinositol; PS, phosphatidylserine; SM, sphingomyelin; SOD, superoxide dismutase; SP, sphingolipid; TP, total protein.</p> Full article ">Figure 4
<p>Adipose tissue proteome analysis. (<b>a</b>) Venn diagram of the identified proteins; (<b>b</b>) PCA score plots of proteome data; (<b>c</b>) volcano plot of the proteome; (<b>d</b>) heatmap of differentially expressed proteins. CON, control; NAR, naringin; FC, fold change.</p> Full article ">Figure 5
<p>Proteomic alteration in adipose tissue samples. GO enrichment analysis of (<b>a</b>) upregulated differentially expressed proteins (DEP) and (<b>b</b>) downregulated DEP; (<b>c</b>) KEGG enrichment analysis of DEP; (<b>d</b>) selected DEP related to sphingolipid metabolism and glycerophospholipid metabolism; (<b>e</b>) selected DEP related to lipolysis and inflammation; (<b>f</b>) selected DEP related to heat stress and extracellular matrix. * <span class="html-italic">p</span> < 0.05, ** <span class="html-italic">p</span> < 0.01, *** <span class="html-italic">p</span> < 0.001, **** <span class="html-italic">p</span> < 0.0001. CON, control; NAR, naringin.</p> Full article ">Figure 6
<p>Integrated pathway and network analysis of the adipose tissue lipidome and proteome. (<b>a</b>) Diagram of lipid metabolism, including glycerolipid metabolism, glycerophospholipid metabolism, and sphingolipid metabolism; (<b>b</b>) protein–protein interaction (PPI) network of selected differentially expressed proteins (DEP); (<b>c</b>) Pearson’s correlation network between differential lipids (glycerophospholipid and sphingolipid species) and selected DEP; red lines represent positive, while blue lines indicate negative correlations (<span class="html-italic">p</span> < 0.05 and |r| > 0.50); (<b>d</b>) Pearson’s correlation analysis between selected DEP and serum biochemical parameters. * <span class="html-italic">p</span> < 0.05, ** <span class="html-italic">p</span> < 0.01. ALT, alanine aminotransferase; AST, aspartate aminotransferase; Cer, ceramide; CL, cardiolipin; CRP, C-reactive protein; dMePE, dimethylphosphatidylethanolamine; GSH-Px, glutathione peroxidase; IL, interleukin; LPS, lipopolysaccharide; MDA, malonaldehyde; NEFA, non-esterified fatty acid; PC, phosphatidylcholine; PE, phosphatidylethanolamine; PI, phosphatidylinositol; PS, phosphatidylserine; SM, sphingomyelin; SOD, superoxide dismutase; TP, total protein.</p> Full article ">
Open AccessArticle
Omega-3-Rich Tuna Oil Derived from By-Products of the Canned Tuna Industry Enhances Memory in an Ovariectomized Rat Model of Menopause
by
Jintanaporn Wattanathorn and Wipawee Thukham-Mee
Antioxidants 2024, 13(6), 637; https://doi.org/10.3390/antiox13060637 - 24 May 2024
Abstract
To increase the value of the by-products of the canned tuna industry, the memory enhancement effect and the possible mechanisms of omega-3-rich tuna oil in bilateral ovariectomized (OVX) rats were assessed. Female rats were orally given tuna oil at doses of 140, 200,
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To increase the value of the by-products of the canned tuna industry, the memory enhancement effect and the possible mechanisms of omega-3-rich tuna oil in bilateral ovariectomized (OVX) rats were assessed. Female rats were orally given tuna oil at doses of 140, 200, and 250 mg/kg of body weight (BW) for 28 days before OVX and for 21 days continually after OVX. Memory performance was assessed every week, whereas the parameters regarding mechanisms of action were assessed at the end of the study. All doses of tuna oil enhanced memory, docosahexaenoic acid (DHA) levels, and superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities but decreased cortisol, acetylcholinesterase (AChE), malondialdehyde (MDA), and inflammatory cytokines such as tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6). Medium and high doses of tuna oil suppressed monoamine oxidase (MAO) but increased eNOS activity. A high dose of tuna oil suppressed gamma-aminotransferase (GABA-T) but increased glutamic acid decarboxylase (GAD) and sirtuin-1. A medium dose of tuna oil decreased homocysteine (Hcys) and C-reactive protein. No change in telomere or estradiol was observed in this study. Our results suggest the memory-enhancing effect of tuna oil in an OVX rat model of menopause. The main mechanisms may involve a reduction in oxidative stress, inflammation, and neurotransmitter regulation.
Full article
(This article belongs to the Section Health Outcomes of Antioxidants and Oxidative Stress)
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Graphical abstract
Full article ">Figure 1
<p>Schematic diagram of the experimental procedure.</p> Full article ">Figure 2
<p>Effect of tuna oil on spatial memory assessed using the Morris water maze test. (<b>A</b>) Effect of tuna oil on escape latency. (<b>B</b>) Effect of tuna oil on retention time (<span class="html-italic">n</span> = 8/group) (data are expressed in mean ± SEM). <sup>a,aaa</sup> <span class="html-italic">p</span>-value < 0.05, 0.001, respectively, compared to the naïve control group; <sup>b,bbb</sup> <span class="html-italic">p</span>-value < 0.05, 0.001, respectively, compared to the DW + sham operation-treated group; <sup>c,ccc</sup> <span class="html-italic">p</span>-value < 0.05, 0.001, respectively, compared to the vehicle + sham operation-treated group *, **, *** <span class="html-italic">p</span>-value < 0.05, 0.01, and 0.001, respectively, compared to the vehicle + OVX-treated group.</p> Full article ">Figure 3
<p>Discrimination index using an object recognition test for various treatment groups at 0.5, 1, and 6 h after substance administration. (<b>A</b>) Discrimination index at 7 days after OVX. (<b>B</b>) Discrimination index at 14 days after OVX. (<b>C</b>) Discrimination index at 21 days after OVX. Data are shown as the mean ± SEM (<span class="html-italic">n</span> = 8). <sup>a,b,c</sup> <span class="html-italic">p</span>-value < 0.05, compared to the naïve control group, the DW + sham operation group, and the vehicle + sham operation group; *, ** <span class="html-italic">p</span>-values < 0.05 and 0.01, respectively, compared to the vehicle + OVX-treated group.</p> Full article ">Figure 3 Cont.
<p>Discrimination index using an object recognition test for various treatment groups at 0.5, 1, and 6 h after substance administration. (<b>A</b>) Discrimination index at 7 days after OVX. (<b>B</b>) Discrimination index at 14 days after OVX. (<b>C</b>) Discrimination index at 21 days after OVX. Data are shown as the mean ± SEM (<span class="html-italic">n</span> = 8). <sup>a,b,c</sup> <span class="html-italic">p</span>-value < 0.05, compared to the naïve control group, the DW + sham operation group, and the vehicle + sham operation group; *, ** <span class="html-italic">p</span>-values < 0.05 and 0.01, respectively, compared to the vehicle + OVX-treated group.</p> Full article ">Figure 4
<p>Acetylcholinesterase activity in the prefrontal cortex of various treatment groups. Data are shown as the mean ± SEM (<span class="html-italic">n</span> = 8/group). <sup>aaa</sup> <span class="html-italic">p</span>-value < 0.001, compared to the naïve control group; <sup>bb</sup> <span class="html-italic">p</span>-value < 0.01, compared to the DW + sham operation group; <sup>cc</sup> <span class="html-italic">p</span>-value < 0.01, compared to the vehicle + sham operation group; and *, **, *** <span class="html-italic">p</span>-values < 0.05, 0.01, and 0.001, respectively, compared to the vehicle + OVX-treated group.</p> Full article ">Figure 5
<p>Monoamine oxidase activity in the prefrontal cortex of various treatment groups. Data are shown as the mean ± SEM (<span class="html-italic">n</span> = 8/group). <sup>aa</sup> <span class="html-italic">p</span>-value < 0.01, compared to the naïve control group; <sup>bb</sup> <span class="html-italic">p</span>-value < 0.01, compared to the DW + sham operation group; <sup>ccc</sup> <span class="html-italic">p</span>-value < 0.001, compared to the vehicle + sham operation group; and *, ** <span class="html-italic">p</span>-values < 0.05 and 0.01, respectively, compared to the vehicle + OVX-treated group.</p> Full article ">Figure 6
<p>Gamma-amino-butyric acid transaminase (GABA-T) enzyme activity in the prefrontal cortex of various treatment groups. Data are shown as the mean ± SEM (<span class="html-italic">n</span> = 8/group). <sup>aaa</sup> <span class="html-italic">p</span>-value < 0.001, compared to the naïve control group; <sup>bb</sup> <span class="html-italic">p</span>-value < 0.01, compared to the DW + sham operation group; <sup>cc</sup> <span class="html-italic">p</span>-value < 0.01, compared to the vehicle + sham operation group; and * <span class="html-italic">p</span>-value < 0.05, compared to the vehicle + OVX-treated group.</p> Full article ">Figure 7
<p>Glutamic acid decarboxylase (GAD) enzyme activity in the prefrontal cortex of various treatment groups. Data are shown as the mean ± SEM (<span class="html-italic">n</span> = 8/group). * <span class="html-italic">p</span>-value < 0.05, compared to the vehicle + OVX-treated group.</p> Full article ">Figure 8
<p>Inflammatory markers, including interleukin-6 (IL-6) (<b>A</b>), tumor necrosis factor-alpha (TNF-α) (<b>B</b>), and C-reactive protein (CRP) (<b>C</b>) in the serum of various treatment groups. Data are shown as the mean ± SEM <b>(</b><span class="html-italic">n</span> = 8/group). <sup>aa,aaa</sup> <span class="html-italic">p</span>-values < 0.01 and 0.001, respectively, compared to the naïve control group; <sup>b,bb,bbb</sup> <span class="html-italic">p</span>-values < 0.05, 0.01, and 0.001, respectively, compared to the DW + sham operation group; <sup>c,ccc</sup> <span class="html-italic">p</span>-values < 0.05 and 0.001, compared to the vehicle + sham operation groups; and *, ** <span class="html-italic">p</span>-values < 0.05 and 0.01, respectively, compared to the vehicle + OVX-treated group.</p> Full article ">Figure 8 Cont.
<p>Inflammatory markers, including interleukin-6 (IL-6) (<b>A</b>), tumor necrosis factor-alpha (TNF-α) (<b>B</b>), and C-reactive protein (CRP) (<b>C</b>) in the serum of various treatment groups. Data are shown as the mean ± SEM <b>(</b><span class="html-italic">n</span> = 8/group). <sup>aa,aaa</sup> <span class="html-italic">p</span>-values < 0.01 and 0.001, respectively, compared to the naïve control group; <sup>b,bb,bbb</sup> <span class="html-italic">p</span>-values < 0.05, 0.01, and 0.001, respectively, compared to the DW + sham operation group; <sup>c,ccc</sup> <span class="html-italic">p</span>-values < 0.05 and 0.001, compared to the vehicle + sham operation groups; and *, ** <span class="html-italic">p</span>-values < 0.05 and 0.01, respectively, compared to the vehicle + OVX-treated group.</p> Full article ">Figure 8 Cont.
<p>Inflammatory markers, including interleukin-6 (IL-6) (<b>A</b>), tumor necrosis factor-alpha (TNF-α) (<b>B</b>), and C-reactive protein (CRP) (<b>C</b>) in the serum of various treatment groups. Data are shown as the mean ± SEM <b>(</b><span class="html-italic">n</span> = 8/group). <sup>aa,aaa</sup> <span class="html-italic">p</span>-values < 0.01 and 0.001, respectively, compared to the naïve control group; <sup>b,bb,bbb</sup> <span class="html-italic">p</span>-values < 0.05, 0.01, and 0.001, respectively, compared to the DW + sham operation group; <sup>c,ccc</sup> <span class="html-italic">p</span>-values < 0.05 and 0.001, compared to the vehicle + sham operation groups; and *, ** <span class="html-italic">p</span>-values < 0.05 and 0.01, respectively, compared to the vehicle + OVX-treated group.</p> Full article ">Figure 9
<p>Levels of estradiol (<b>A</b>) and cortisol (<b>B</b>) in the serum of various treatment groups. Data are shown as the mean ± SEM (<span class="html-italic">n</span> = 8/group). <sup>a,aa</sup> <span class="html-italic">p</span>-values < 0.05 and 0.01, respectively, compared to the naïve control group; <sup>b,bbb</sup> <span class="html-italic">p</span>-values < 0.05 and 0.001, respectively, compared to the DW + sham operation group; <sup>c</sup> <span class="html-italic">p</span>-value < 0.05 compared to the vehicle + sham operation group; and *, ** <span class="html-italic">p</span>-values < 0.05 and 0.01, respectively, compared to the vehicle + OVX-treated group.</p> Full article ">Figure 9 Cont.
<p>Levels of estradiol (<b>A</b>) and cortisol (<b>B</b>) in the serum of various treatment groups. Data are shown as the mean ± SEM (<span class="html-italic">n</span> = 8/group). <sup>a,aa</sup> <span class="html-italic">p</span>-values < 0.05 and 0.01, respectively, compared to the naïve control group; <sup>b,bbb</sup> <span class="html-italic">p</span>-values < 0.05 and 0.001, respectively, compared to the DW + sham operation group; <sup>c</sup> <span class="html-italic">p</span>-value < 0.05 compared to the vehicle + sham operation group; and *, ** <span class="html-italic">p</span>-values < 0.05 and 0.01, respectively, compared to the vehicle + OVX-treated group.</p> Full article ">Figure 10
<p>Changes in various surrogate markers, including homocysteine (Hcys) (<b>A</b>), endothelial nitric oxide synthase (eNOS) (<b>B</b>), siruin-1 (sirt-1) (<b>C</b>), and telomere length (<b>D</b>), in various treatment groups. Data are shown as the mean ± SEM (<span class="html-italic">n</span> = 8/group)<sup>.</sup> *, ** <span class="html-italic">p</span>-values < 0.05 and 0.01, respectively, compared to the vehicle + OVX-treated group.</p> Full article ">Figure 10 Cont.
<p>Changes in various surrogate markers, including homocysteine (Hcys) (<b>A</b>), endothelial nitric oxide synthase (eNOS) (<b>B</b>), siruin-1 (sirt-1) (<b>C</b>), and telomere length (<b>D</b>), in various treatment groups. Data are shown as the mean ± SEM (<span class="html-italic">n</span> = 8/group)<sup>.</sup> *, ** <span class="html-italic">p</span>-values < 0.05 and 0.01, respectively, compared to the vehicle + OVX-treated group.</p> Full article ">Figure 10 Cont.
<p>Changes in various surrogate markers, including homocysteine (Hcys) (<b>A</b>), endothelial nitric oxide synthase (eNOS) (<b>B</b>), siruin-1 (sirt-1) (<b>C</b>), and telomere length (<b>D</b>), in various treatment groups. Data are shown as the mean ± SEM (<span class="html-italic">n</span> = 8/group)<sup>.</sup> *, ** <span class="html-italic">p</span>-values < 0.05 and 0.01, respectively, compared to the vehicle + OVX-treated group.</p> Full article ">Figure 10 Cont.
<p>Changes in various surrogate markers, including homocysteine (Hcys) (<b>A</b>), endothelial nitric oxide synthase (eNOS) (<b>B</b>), siruin-1 (sirt-1) (<b>C</b>), and telomere length (<b>D</b>), in various treatment groups. Data are shown as the mean ± SEM (<span class="html-italic">n</span> = 8/group)<sup>.</sup> *, ** <span class="html-italic">p</span>-values < 0.05 and 0.01, respectively, compared to the vehicle + OVX-treated group.</p> Full article ">Figure 11
<p>Serum levels of docosahexaenoic acid (DHA) in various treatment groups. Data are shown as the mean ± SEM (<span class="html-italic">n</span> = 8/group). *, ** <span class="html-italic">p</span>-values < 0.05 and 0.01, respectively, compared to the vehicle + OVX-treated group.</p> Full article ">
Full article ">Figure 1
<p>Schematic diagram of the experimental procedure.</p> Full article ">Figure 2
<p>Effect of tuna oil on spatial memory assessed using the Morris water maze test. (<b>A</b>) Effect of tuna oil on escape latency. (<b>B</b>) Effect of tuna oil on retention time (<span class="html-italic">n</span> = 8/group) (data are expressed in mean ± SEM). <sup>a,aaa</sup> <span class="html-italic">p</span>-value < 0.05, 0.001, respectively, compared to the naïve control group; <sup>b,bbb</sup> <span class="html-italic">p</span>-value < 0.05, 0.001, respectively, compared to the DW + sham operation-treated group; <sup>c,ccc</sup> <span class="html-italic">p</span>-value < 0.05, 0.001, respectively, compared to the vehicle + sham operation-treated group *, **, *** <span class="html-italic">p</span>-value < 0.05, 0.01, and 0.001, respectively, compared to the vehicle + OVX-treated group.</p> Full article ">Figure 3
<p>Discrimination index using an object recognition test for various treatment groups at 0.5, 1, and 6 h after substance administration. (<b>A</b>) Discrimination index at 7 days after OVX. (<b>B</b>) Discrimination index at 14 days after OVX. (<b>C</b>) Discrimination index at 21 days after OVX. Data are shown as the mean ± SEM (<span class="html-italic">n</span> = 8). <sup>a,b,c</sup> <span class="html-italic">p</span>-value < 0.05, compared to the naïve control group, the DW + sham operation group, and the vehicle + sham operation group; *, ** <span class="html-italic">p</span>-values < 0.05 and 0.01, respectively, compared to the vehicle + OVX-treated group.</p> Full article ">Figure 3 Cont.
<p>Discrimination index using an object recognition test for various treatment groups at 0.5, 1, and 6 h after substance administration. (<b>A</b>) Discrimination index at 7 days after OVX. (<b>B</b>) Discrimination index at 14 days after OVX. (<b>C</b>) Discrimination index at 21 days after OVX. Data are shown as the mean ± SEM (<span class="html-italic">n</span> = 8). <sup>a,b,c</sup> <span class="html-italic">p</span>-value < 0.05, compared to the naïve control group, the DW + sham operation group, and the vehicle + sham operation group; *, ** <span class="html-italic">p</span>-values < 0.05 and 0.01, respectively, compared to the vehicle + OVX-treated group.</p> Full article ">Figure 4
<p>Acetylcholinesterase activity in the prefrontal cortex of various treatment groups. Data are shown as the mean ± SEM (<span class="html-italic">n</span> = 8/group). <sup>aaa</sup> <span class="html-italic">p</span>-value < 0.001, compared to the naïve control group; <sup>bb</sup> <span class="html-italic">p</span>-value < 0.01, compared to the DW + sham operation group; <sup>cc</sup> <span class="html-italic">p</span>-value < 0.01, compared to the vehicle + sham operation group; and *, **, *** <span class="html-italic">p</span>-values < 0.05, 0.01, and 0.001, respectively, compared to the vehicle + OVX-treated group.</p> Full article ">Figure 5
<p>Monoamine oxidase activity in the prefrontal cortex of various treatment groups. Data are shown as the mean ± SEM (<span class="html-italic">n</span> = 8/group). <sup>aa</sup> <span class="html-italic">p</span>-value < 0.01, compared to the naïve control group; <sup>bb</sup> <span class="html-italic">p</span>-value < 0.01, compared to the DW + sham operation group; <sup>ccc</sup> <span class="html-italic">p</span>-value < 0.001, compared to the vehicle + sham operation group; and *, ** <span class="html-italic">p</span>-values < 0.05 and 0.01, respectively, compared to the vehicle + OVX-treated group.</p> Full article ">Figure 6
<p>Gamma-amino-butyric acid transaminase (GABA-T) enzyme activity in the prefrontal cortex of various treatment groups. Data are shown as the mean ± SEM (<span class="html-italic">n</span> = 8/group). <sup>aaa</sup> <span class="html-italic">p</span>-value < 0.001, compared to the naïve control group; <sup>bb</sup> <span class="html-italic">p</span>-value < 0.01, compared to the DW + sham operation group; <sup>cc</sup> <span class="html-italic">p</span>-value < 0.01, compared to the vehicle + sham operation group; and * <span class="html-italic">p</span>-value < 0.05, compared to the vehicle + OVX-treated group.</p> Full article ">Figure 7
<p>Glutamic acid decarboxylase (GAD) enzyme activity in the prefrontal cortex of various treatment groups. Data are shown as the mean ± SEM (<span class="html-italic">n</span> = 8/group). * <span class="html-italic">p</span>-value < 0.05, compared to the vehicle + OVX-treated group.</p> Full article ">Figure 8
<p>Inflammatory markers, including interleukin-6 (IL-6) (<b>A</b>), tumor necrosis factor-alpha (TNF-α) (<b>B</b>), and C-reactive protein (CRP) (<b>C</b>) in the serum of various treatment groups. Data are shown as the mean ± SEM <b>(</b><span class="html-italic">n</span> = 8/group). <sup>aa,aaa</sup> <span class="html-italic">p</span>-values < 0.01 and 0.001, respectively, compared to the naïve control group; <sup>b,bb,bbb</sup> <span class="html-italic">p</span>-values < 0.05, 0.01, and 0.001, respectively, compared to the DW + sham operation group; <sup>c,ccc</sup> <span class="html-italic">p</span>-values < 0.05 and 0.001, compared to the vehicle + sham operation groups; and *, ** <span class="html-italic">p</span>-values < 0.05 and 0.01, respectively, compared to the vehicle + OVX-treated group.</p> Full article ">Figure 8 Cont.
<p>Inflammatory markers, including interleukin-6 (IL-6) (<b>A</b>), tumor necrosis factor-alpha (TNF-α) (<b>B</b>), and C-reactive protein (CRP) (<b>C</b>) in the serum of various treatment groups. Data are shown as the mean ± SEM <b>(</b><span class="html-italic">n</span> = 8/group). <sup>aa,aaa</sup> <span class="html-italic">p</span>-values < 0.01 and 0.001, respectively, compared to the naïve control group; <sup>b,bb,bbb</sup> <span class="html-italic">p</span>-values < 0.05, 0.01, and 0.001, respectively, compared to the DW + sham operation group; <sup>c,ccc</sup> <span class="html-italic">p</span>-values < 0.05 and 0.001, compared to the vehicle + sham operation groups; and *, ** <span class="html-italic">p</span>-values < 0.05 and 0.01, respectively, compared to the vehicle + OVX-treated group.</p> Full article ">Figure 8 Cont.
<p>Inflammatory markers, including interleukin-6 (IL-6) (<b>A</b>), tumor necrosis factor-alpha (TNF-α) (<b>B</b>), and C-reactive protein (CRP) (<b>C</b>) in the serum of various treatment groups. Data are shown as the mean ± SEM <b>(</b><span class="html-italic">n</span> = 8/group). <sup>aa,aaa</sup> <span class="html-italic">p</span>-values < 0.01 and 0.001, respectively, compared to the naïve control group; <sup>b,bb,bbb</sup> <span class="html-italic">p</span>-values < 0.05, 0.01, and 0.001, respectively, compared to the DW + sham operation group; <sup>c,ccc</sup> <span class="html-italic">p</span>-values < 0.05 and 0.001, compared to the vehicle + sham operation groups; and *, ** <span class="html-italic">p</span>-values < 0.05 and 0.01, respectively, compared to the vehicle + OVX-treated group.</p> Full article ">Figure 9
<p>Levels of estradiol (<b>A</b>) and cortisol (<b>B</b>) in the serum of various treatment groups. Data are shown as the mean ± SEM (<span class="html-italic">n</span> = 8/group). <sup>a,aa</sup> <span class="html-italic">p</span>-values < 0.05 and 0.01, respectively, compared to the naïve control group; <sup>b,bbb</sup> <span class="html-italic">p</span>-values < 0.05 and 0.001, respectively, compared to the DW + sham operation group; <sup>c</sup> <span class="html-italic">p</span>-value < 0.05 compared to the vehicle + sham operation group; and *, ** <span class="html-italic">p</span>-values < 0.05 and 0.01, respectively, compared to the vehicle + OVX-treated group.</p> Full article ">Figure 9 Cont.
<p>Levels of estradiol (<b>A</b>) and cortisol (<b>B</b>) in the serum of various treatment groups. Data are shown as the mean ± SEM (<span class="html-italic">n</span> = 8/group). <sup>a,aa</sup> <span class="html-italic">p</span>-values < 0.05 and 0.01, respectively, compared to the naïve control group; <sup>b,bbb</sup> <span class="html-italic">p</span>-values < 0.05 and 0.001, respectively, compared to the DW + sham operation group; <sup>c</sup> <span class="html-italic">p</span>-value < 0.05 compared to the vehicle + sham operation group; and *, ** <span class="html-italic">p</span>-values < 0.05 and 0.01, respectively, compared to the vehicle + OVX-treated group.</p> Full article ">Figure 10
<p>Changes in various surrogate markers, including homocysteine (Hcys) (<b>A</b>), endothelial nitric oxide synthase (eNOS) (<b>B</b>), siruin-1 (sirt-1) (<b>C</b>), and telomere length (<b>D</b>), in various treatment groups. Data are shown as the mean ± SEM (<span class="html-italic">n</span> = 8/group)<sup>.</sup> *, ** <span class="html-italic">p</span>-values < 0.05 and 0.01, respectively, compared to the vehicle + OVX-treated group.</p> Full article ">Figure 10 Cont.
<p>Changes in various surrogate markers, including homocysteine (Hcys) (<b>A</b>), endothelial nitric oxide synthase (eNOS) (<b>B</b>), siruin-1 (sirt-1) (<b>C</b>), and telomere length (<b>D</b>), in various treatment groups. Data are shown as the mean ± SEM (<span class="html-italic">n</span> = 8/group)<sup>.</sup> *, ** <span class="html-italic">p</span>-values < 0.05 and 0.01, respectively, compared to the vehicle + OVX-treated group.</p> Full article ">Figure 10 Cont.
<p>Changes in various surrogate markers, including homocysteine (Hcys) (<b>A</b>), endothelial nitric oxide synthase (eNOS) (<b>B</b>), siruin-1 (sirt-1) (<b>C</b>), and telomere length (<b>D</b>), in various treatment groups. Data are shown as the mean ± SEM (<span class="html-italic">n</span> = 8/group)<sup>.</sup> *, ** <span class="html-italic">p</span>-values < 0.05 and 0.01, respectively, compared to the vehicle + OVX-treated group.</p> Full article ">Figure 10 Cont.
<p>Changes in various surrogate markers, including homocysteine (Hcys) (<b>A</b>), endothelial nitric oxide synthase (eNOS) (<b>B</b>), siruin-1 (sirt-1) (<b>C</b>), and telomere length (<b>D</b>), in various treatment groups. Data are shown as the mean ± SEM (<span class="html-italic">n</span> = 8/group)<sup>.</sup> *, ** <span class="html-italic">p</span>-values < 0.05 and 0.01, respectively, compared to the vehicle + OVX-treated group.</p> Full article ">Figure 11
<p>Serum levels of docosahexaenoic acid (DHA) in various treatment groups. Data are shown as the mean ± SEM (<span class="html-italic">n</span> = 8/group). *, ** <span class="html-italic">p</span>-values < 0.05 and 0.01, respectively, compared to the vehicle + OVX-treated group.</p> Full article ">
Open AccessReview
Unlocking the Nutraceutical Potential of Legumes and Their By-Products: Paving the Way for the Circular Economy in the Agri-Food Industry
by
Fanghua Guo, Renan Danielski, Sarusha Santhiravel and Fereidoon Shahidi
Antioxidants 2024, 13(6), 636; https://doi.org/10.3390/antiox13060636 - 24 May 2024
Abstract
Legumes, including beans, peas, chickpeas, and lentils, are cultivated worldwide and serve as important components of a balanced and nutritious diet. Each legume variety contains unique levels of protein, starch, fiber, lipids, minerals, and vitamins, with potential applications in various industries. By-products such
[...] Read more.
Legumes, including beans, peas, chickpeas, and lentils, are cultivated worldwide and serve as important components of a balanced and nutritious diet. Each legume variety contains unique levels of protein, starch, fiber, lipids, minerals, and vitamins, with potential applications in various industries. By-products such as hulls, rich in bioactive compounds, offer promise for value-added utilization and health-focused product development. Various extraction methods are employed to enhance protein extraction rates from legume by-products, finding applications in various foods such as meat analogs, breads, and desserts. Moreover, essential fatty acids, carotenoids, tocols, and polyphenols are abundant in several residual fractions from legumes. These bioactive classes are linked to reduced incidence of cardiovascular diseases, chronic inflammation, some cancers, obesity, and type 2 diabetes, among other relevant health conditions. The present contribution provides a comprehensive review of the nutritional and bioactive composition of major legumes and their by-products. Additionally, the bioaccessibility and bioavailability aspects of legume consumption, as well as in vitro and in vivo evidence of their health effects are addressed.
Full article
(This article belongs to the Special Issue Legume Antioxidants: Chemistry and Potential Health Impact as Affected by Food Processing and Storage)
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Figure 1
Figure 1
<p>Yield and main producing countries for the major legumes cultivated in the world. Created with Bio Render.</p> Full article ">Figure 2
<p>Thermal and non-thermal processing techniques used to increase the bioefficiency of legume bioactives. Created with Bio Render.</p> Full article ">Figure 3
<p>Main health benefits associated with the consumption of bioactive compounds contained in legume by-products. Created with Bio Render.</p> Full article ">
<p>Yield and main producing countries for the major legumes cultivated in the world. Created with Bio Render.</p> Full article ">Figure 2
<p>Thermal and non-thermal processing techniques used to increase the bioefficiency of legume bioactives. Created with Bio Render.</p> Full article ">Figure 3
<p>Main health benefits associated with the consumption of bioactive compounds contained in legume by-products. Created with Bio Render.</p> Full article ">
Open AccessArticle
Micronutrient Antioxidants for Men (Menevit®) Improve Sperm Function by Reducing Oxidative Stress, Resulting in Improved Assisted Reproductive Technology Outcomes
by
Seiji Ogawa, Kuniaki Ota, Kaori Nishizawa, Masumi Shinagawa, Mikiko Katagiri, Hiroyuki Kikuchi, Hideyuki Kobayashi, Toshifumi Takahashi and Hiroaki Yoshida
Antioxidants 2024, 13(6), 635; https://doi.org/10.3390/antiox13060635 - 23 May 2024
Abstract
Oxidative stress (OS) affects men’s health and impairs spermatogenesis. Micronutrient antioxidants are available for male infertility as complemental support; however, their efficacy remains debatable. This study aimed to investigate whether antioxidants can help to reduce sperm OS and improve semen analysis and quality.
[...] Read more.
Oxidative stress (OS) affects men’s health and impairs spermatogenesis. Micronutrient antioxidants are available for male infertility as complemental support; however, their efficacy remains debatable. This study aimed to investigate whether antioxidants can help to reduce sperm OS and improve semen analysis and quality. We included 171 male partners of couples planning to undergo assisted reproductive technology (ART). Male partners, aged 29–41 years, of couples intending to conceive were self-selected to take daily antioxidants (n = 84) containing folic acid and zinc, or not to take antioxidants (n = 52) for 6 months. We analyzed the alterations in serum oxidant levels, sperm parameters, OS, and deoxyribonucleic acid fragmentation after 3 and 6 months. Additionally, implantation, clinical pregnancy, and miscarriage rates after vitrified–warmed embryo transfer were compared between those taking antioxidants and those not taking them after 6 months. In men with high static oxidation–reduction potential (sORP), we observed a significant improvement in sperm concentration and sORP. The high-quality blastocyst rate tended to increase, and implantation and clinical pregnancy rates also significantly increased after 6 months of intervention. The micronutrient antioxidants could improve sperm function by reducing OS and improving ART outcomes. Therefore, micronutrient antioxidants may be a viable treatment option for male infertility.
Full article
(This article belongs to the Special Issue Effect of Oxidative Stress on Reproduction and Development—2nd Edition)
Open AccessReview
Ischemic Brain Injury: Involvement of Lipids in the Pathophysiology of Stroke and Therapeutic Strategies
by
Nathalie Bernoud-Hubac, Amanda Lo Van, Adina-Nicoleta Lazar and Michel Lagarde
Antioxidants 2024, 13(6), 634; https://doi.org/10.3390/antiox13060634 - 23 May 2024
Abstract
Stroke is a devastating neurological disorder that is characterized by the sudden disruption of blood flow to the brain. Lipids are essential components of brain structure and function and play pivotal roles in stroke pathophysiology. Dysregulation of lipid signaling pathways modulates key cellular
[...] Read more.
Stroke is a devastating neurological disorder that is characterized by the sudden disruption of blood flow to the brain. Lipids are essential components of brain structure and function and play pivotal roles in stroke pathophysiology. Dysregulation of lipid signaling pathways modulates key cellular processes such as apoptosis, inflammation, and oxidative stress, exacerbating ischemic brain injury. In the present review, we summarize the roles of lipids in stroke pathology in different models (cell cultures, animal, and human studies). Additionally, the potential of lipids, especially polyunsaturated fatty acids, to promote neuroprotection and their use as biomarkers in stroke are discussed.
Full article
(This article belongs to the Special Issue Oxidative Stress and Antioxidants in Hypoxia and Human Pathophysiology Settings: Novel Pharmacological Targets)
Open AccessArticle
Photobiomodulation Inhibits Ischemia-Induced Brain Endothelial Senescence via Endothelial Nitric Oxide Synthase
by
Yu Feng, Zhihai Huang, Xiaohui Ma, Xuemei Zong, Vesna Tesic, Baojin Ding, Celeste Yin-Chieh Wu, Reggie Hui-Chao Lee and Quanguang Zhang
Antioxidants 2024, 13(6), 633; https://doi.org/10.3390/antiox13060633 - 23 May 2024
Abstract
Recent research suggests that photobiomodulation therapy (PBMT) positively impacts the vascular function associated with various cerebrovascular diseases. Nevertheless, the specific mechanisms by which PBMT improves vascular function remain ambiguous. Since endothelial nitric oxide synthase (eNOS) is crucial in regulating vascular function following cerebral
[...] Read more.
Recent research suggests that photobiomodulation therapy (PBMT) positively impacts the vascular function associated with various cerebrovascular diseases. Nevertheless, the specific mechanisms by which PBMT improves vascular function remain ambiguous. Since endothelial nitric oxide synthase (eNOS) is crucial in regulating vascular function following cerebral ischemia, we investigated whether eNOS is a key element controlling cerebrovascular function and the senescence of vascular endothelial cells following PBMT treatment. Both rat photothrombotic (PT) stroke and in vitro oxygen–glucose deprivation (OGD)-induced vascular endothelial injury models were utilized. We demonstrated that treatment with PBMT (808 nm, 350 mW/cm2, 2 min/day) for 7 days significantly reduced PT-stroke-induced vascular permeability. Additionally, PBMT inhibited the levels of endothelial senescence markers (senescence green and p21) and antiangiogenic factor (endostatin), while increasing the phospho-eNOS (Ser1177) in the peri-infarct region following PT stroke. In vitro study further indicated that OGD increased p21, endostatin, and DNA damage (γH2AX) levels in the brain endothelial cell line, but they were reversed by PBMT. Intriguingly, the beneficial effects of PBMT were attenuated by a NOS inhibitor. In summary, these findings provide novel insights into the role of eNOS in PBMT-mediated protection against cerebrovascular senescence and endothelial dysfunction following ischemia. The use of PBMT as a therapeutic is a promising strategy to improve endothelial function in cerebrovascular disease.
Full article
(This article belongs to the Special Issue Oxidative Stress and Pathophysiology of Stroke)
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Figure 1
Figure 1
<p>Schematic diagram. (<b>A</b>) The experimental procedure for culturing the bEnd.3 cells. (<b>B</b>) Experimental timeline for animal experiments.</p> Full article ">Figure 2
<p>PBMT diminished the blood–brain barrier (BBB) permeability and decreased endostatin levels in PTstroke rats. (<b>A</b>) Representative fluorescence images of Evans blue (red), endostatin (green), and Reca1 (red) in the peri-infarct zone. Nuclei were counterstained with DAPI (blue). (<b>B</b>,<b>C</b>) Quantitative analysis of Evans blue leakage and vessel-associated endostatin was performed using ImageJ software (n = 5–6). The data were expressed as percentage changes versus the respective sham group. * indicates <span class="html-italic">p</span> < 0.05 vs. sham group; # indicates <span class="html-italic">p</span> < 0.05 vs. PT-stroke group. Scale bar = 20 μm.</p> Full article ">Figure 3
<p>PBMT inhibited cerebrovascular senescence in PT-stroke rats. (<b>A</b>) Representative fluorescence images of senescence green (green), P21 (green), and CD31 (red) in the peri-infarct zone. Nuclei were counterstained with DAPI (blue). (<b>B</b>,<b>C</b>) Quantitative analysis of vessel-associated senescence green and P21 in the peri-infarct zone of rats. The data were expressed as percentage changes versus the respective Sham group. * indicates <span class="html-italic">p</span> < 0.05 vs. sham group; # indicates <span class="html-italic">p</span> < 0.05 vs. PT-stroke group. Scale bar = 20 μm.</p> Full article ">Figure 4
<p>PBMT increased the phosphorylation of eNOS at Ser-1177 in PT-stroke rats and OGD-exposed bEnd.3 cells. (<b>A</b>) Representative fluorescence images of p-eNOS (green) in the peri-infarct zone. (<b>B</b>) Quantitative analysis of p-eNOS fluorescence intensity in the peri-infarct zone of rats. The data were expressed as percentage changes versus the respective sham group. Scale bar = 50 μm. (<b>C</b>) Representative immunofluorescence images for p-eNOS (green). (<b>D</b>) p-eNOS intensity was calculated and expressed as percentage changes relative to the control group. Scale bar = 50 µm (n = 6). * indicates <span class="html-italic">p</span> < 0.05 vs. sham or control group; # indicates <span class="html-italic">p</span> < 0.05 vs. PT-stroke or OGD group.</p> Full article ">Figure 5
<p>Effect of L-NAME on the cell viability and endostatin level in bEnd.3 cells. (<b>A</b>,<b>B</b>) MTT assay was used to measure viability in bEnd.3 cells after treatment with L-NAME at 1 μM to 1000 mM concentrations in bEnd.3 cells. The data are expressed as mean ± SD (n = 5–6). (<b>C</b>) Representative fluorescence images of endostatin (green) in the bEnd.3 cells. (<b>D</b>) Quantitative analysis of endostatin intensity. The data were expressed as percentage changes versus the respective control group. (n = 5–6). * indicates <span class="html-italic">p</span> < 0.05 vs. control group; # indicates <span class="html-italic">p</span> < 0.05 vs. OGD group. & indicates <span class="html-italic">p</span> < 0.05 vs. OGD + PBMT group. Scale bar = 20 μm.</p> Full article ">Figure 6
<p>Pretreatment with L-NAME prevented PBMT-inhibited cellular senescence in bEnd.3 cells. (<b>A</b>) Representative fluorescence images of P21 (green) in the bEnd.3 cells. Nuclei were counterstained with DAPI (blue). (<b>B</b>) P21 staining intensity was analyzed and expressed as percentage changes versus the control group. (<b>C</b>,<b>D</b>) Western blotting and quantitative analysis of P21 levels using protein samples from bEnd.3 cells (n = 3–6). * indicates <span class="html-italic">p</span> < 0.05 vs. control group; # indicates <span class="html-italic">p</span> < 0.05 vs. OGD group. & indicates <span class="html-italic">p</span> < 0.05 vs. OGD + PBMT group. Scale bar = 20 μm.</p> Full article ">Figure 7
<p>Pretreatment with L-NAME prevented a PBMT-induced decrease in histone H2AX phosphorylation in bEnd.3 cells. (<b>A</b>) Representative immunofluorescence images for γH2AX (purple). Nuclei were counterstained with DAPI (blue). (<b>B</b>) The ratio of γH2AX+ cell and total cell numbers was calculated and expressed as percentage changes relative to the control group. Scale bar = 50 µm (n = 6). * indicates <span class="html-italic">p</span> < 0.05 vs. control group; # indicates <span class="html-italic">p</span> < 0.05 vs. OGD group. & indicates <span class="html-italic">p</span> < 0.05 vs. OGD + PBMT group.</p> Full article ">Figure 8
<p>Graphical abstract. OGD or ischemic stroke inhibits the phosphorylation of eNOS, induces histone H2AX phosphorylation, and causes cerebrovascular senescence. Conversely, PBMT promotes the phosphorylation of eNOS, induces cell proliferation, and inhibits cerebrovascular senescence.</p> Full article ">
<p>Schematic diagram. (<b>A</b>) The experimental procedure for culturing the bEnd.3 cells. (<b>B</b>) Experimental timeline for animal experiments.</p> Full article ">Figure 2
<p>PBMT diminished the blood–brain barrier (BBB) permeability and decreased endostatin levels in PTstroke rats. (<b>A</b>) Representative fluorescence images of Evans blue (red), endostatin (green), and Reca1 (red) in the peri-infarct zone. Nuclei were counterstained with DAPI (blue). (<b>B</b>,<b>C</b>) Quantitative analysis of Evans blue leakage and vessel-associated endostatin was performed using ImageJ software (n = 5–6). The data were expressed as percentage changes versus the respective sham group. * indicates <span class="html-italic">p</span> < 0.05 vs. sham group; # indicates <span class="html-italic">p</span> < 0.05 vs. PT-stroke group. Scale bar = 20 μm.</p> Full article ">Figure 3
<p>PBMT inhibited cerebrovascular senescence in PT-stroke rats. (<b>A</b>) Representative fluorescence images of senescence green (green), P21 (green), and CD31 (red) in the peri-infarct zone. Nuclei were counterstained with DAPI (blue). (<b>B</b>,<b>C</b>) Quantitative analysis of vessel-associated senescence green and P21 in the peri-infarct zone of rats. The data were expressed as percentage changes versus the respective Sham group. * indicates <span class="html-italic">p</span> < 0.05 vs. sham group; # indicates <span class="html-italic">p</span> < 0.05 vs. PT-stroke group. Scale bar = 20 μm.</p> Full article ">Figure 4
<p>PBMT increased the phosphorylation of eNOS at Ser-1177 in PT-stroke rats and OGD-exposed bEnd.3 cells. (<b>A</b>) Representative fluorescence images of p-eNOS (green) in the peri-infarct zone. (<b>B</b>) Quantitative analysis of p-eNOS fluorescence intensity in the peri-infarct zone of rats. The data were expressed as percentage changes versus the respective sham group. Scale bar = 50 μm. (<b>C</b>) Representative immunofluorescence images for p-eNOS (green). (<b>D</b>) p-eNOS intensity was calculated and expressed as percentage changes relative to the control group. Scale bar = 50 µm (n = 6). * indicates <span class="html-italic">p</span> < 0.05 vs. sham or control group; # indicates <span class="html-italic">p</span> < 0.05 vs. PT-stroke or OGD group.</p> Full article ">Figure 5
<p>Effect of L-NAME on the cell viability and endostatin level in bEnd.3 cells. (<b>A</b>,<b>B</b>) MTT assay was used to measure viability in bEnd.3 cells after treatment with L-NAME at 1 μM to 1000 mM concentrations in bEnd.3 cells. The data are expressed as mean ± SD (n = 5–6). (<b>C</b>) Representative fluorescence images of endostatin (green) in the bEnd.3 cells. (<b>D</b>) Quantitative analysis of endostatin intensity. The data were expressed as percentage changes versus the respective control group. (n = 5–6). * indicates <span class="html-italic">p</span> < 0.05 vs. control group; # indicates <span class="html-italic">p</span> < 0.05 vs. OGD group. & indicates <span class="html-italic">p</span> < 0.05 vs. OGD + PBMT group. Scale bar = 20 μm.</p> Full article ">Figure 6
<p>Pretreatment with L-NAME prevented PBMT-inhibited cellular senescence in bEnd.3 cells. (<b>A</b>) Representative fluorescence images of P21 (green) in the bEnd.3 cells. Nuclei were counterstained with DAPI (blue). (<b>B</b>) P21 staining intensity was analyzed and expressed as percentage changes versus the control group. (<b>C</b>,<b>D</b>) Western blotting and quantitative analysis of P21 levels using protein samples from bEnd.3 cells (n = 3–6). * indicates <span class="html-italic">p</span> < 0.05 vs. control group; # indicates <span class="html-italic">p</span> < 0.05 vs. OGD group. & indicates <span class="html-italic">p</span> < 0.05 vs. OGD + PBMT group. Scale bar = 20 μm.</p> Full article ">Figure 7
<p>Pretreatment with L-NAME prevented a PBMT-induced decrease in histone H2AX phosphorylation in bEnd.3 cells. (<b>A</b>) Representative immunofluorescence images for γH2AX (purple). Nuclei were counterstained with DAPI (blue). (<b>B</b>) The ratio of γH2AX+ cell and total cell numbers was calculated and expressed as percentage changes relative to the control group. Scale bar = 50 µm (n = 6). * indicates <span class="html-italic">p</span> < 0.05 vs. control group; # indicates <span class="html-italic">p</span> < 0.05 vs. OGD group. & indicates <span class="html-italic">p</span> < 0.05 vs. OGD + PBMT group.</p> Full article ">Figure 8
<p>Graphical abstract. OGD or ischemic stroke inhibits the phosphorylation of eNOS, induces histone H2AX phosphorylation, and causes cerebrovascular senescence. Conversely, PBMT promotes the phosphorylation of eNOS, induces cell proliferation, and inhibits cerebrovascular senescence.</p> Full article ">
Open AccessArticle
Mechanism of Action of Isoflavone Derived from Soy-Based Tempeh as an Antioxidant and Breast Cancer Inhibitor via Potential Upregulation of miR-7-5p: A Multimodal Analysis Integrating Pharmacoinformatics and Cellular Studies
by
Fahrul Nurkolis, Nurpudji Astuti Taslim, Dain Lee, Moon Nyeo Park, Seungjoon Moon, Hardinsyah Hardinsyah, Raymond Rubianto Tjandrawinata, Nelly Mayulu, Made Astawan, Trina Ekawati Tallei and Bonglee Kim
Antioxidants 2024, 13(6), 632; https://doi.org/10.3390/antiox13060632 - 22 May 2024
Abstract
Breast cancer presents a significant global health challenge with rising incidence rates worldwide. Despite current efforts, it remains inadequately controlled. Functional foods, notably tempeh, have emerged as promising candidates for breast cancer prevention and treatment due to bioactive peptides and isoflavones exhibiting potential
[...] Read more.
Breast cancer presents a significant global health challenge with rising incidence rates worldwide. Despite current efforts, it remains inadequately controlled. Functional foods, notably tempeh, have emerged as promising candidates for breast cancer prevention and treatment due to bioactive peptides and isoflavones exhibiting potential anticancer properties by serving as antioxidants, inducing apoptosis, and inhibiting cancer cell proliferation. This study integrates pharmacoinformatics and cellular investigations (i.e., a multifaceted approach) to elucidate the antioxidative and anti-breast cancer properties of tempeh-derived isoflavones. Methodologies encompass metabolomic profiling, in silico analysis, antioxidant assays, and in vitro experiments. Daidzein and genistein exhibited potential therapeutic options for breast cancer treatment and as antioxidant agents. In vitro studies also supported their efficacy against breast cancer and their ability to scavenge radicals, particularly in soy-based tempeh powder (SBT-P) and its isoflavone derivatives. Results have demonstrated a significant downregulation of breast cancer signaling proteins and increased expression of miR-7-5p, a microRNA with tumor-suppressive properties. Notably, the LD50 values of SBT-P and its derivatives on normal breast cell lines indicate their potential safety, with minimal cytotoxic effects on MCF-10A cells compared to control groups. The study underscores the favorable potential of SBT-P as a safe therapeutic option for breast cancer treatment, warranting further clinical exploration.
Full article
(This article belongs to the Special Issue Role of Natural Antioxidants in Cardiovascular Diseases and Cancers)
Open AccessEditorial
Anti-Oxidative Bioactivities of Medicinal Herbs in the Treatment of Aging-Related Diseases
by
Hye-Sun Lim, Gunhyuk Park and Yong-Ung Kim
Antioxidants 2024, 13(6), 631; https://doi.org/10.3390/antiox13060631 - 22 May 2024
Abstract
Over the last 20 years, significant progress has been made in understanding the biology of aging and lifespans [...]
Full article
(This article belongs to the Special Issue Anti-Oxidative Bioactivities of Medicinal Herbs for Treatment of Aging-Related Diseases)
Open AccessCommunication
Improved Antioxidant Blood Parameters in Piglets Fed Diets Containing Solid-State Fermented Mixture of Olive Mill Stone Waste and Lathyrus clymenum Husks
by
Christos Eliopoulos, George Papadomichelakis, Arina Voitova, Nikos Chorianopoulos, Serkos A. Haroutounian, Giorgos Markou and Dimitrios Arapoglou
Antioxidants 2024, 13(6), 630; https://doi.org/10.3390/antiox13060630 - 22 May 2024
Abstract
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Show Figures
Solid-state fermentation represents a sustainable approach for the conversion of agro-industrial wastes into high-added-value feed ingredients. The present study aimed to evaluate the effects of the dietary addition of a solid-state-fermented mixture of olive mill stone waste (OMSW) and Lathyrus clymenum husks (LP)
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Solid-state fermentation represents a sustainable approach for the conversion of agro-industrial wastes into high-added-value feed ingredients. The present study aimed to evaluate the effects of the dietary addition of a solid-state-fermented mixture of olive mill stone waste (OMSW) and Lathyrus clymenum husks (LP) on the antioxidant blood parameters of weaned piglets. Two hundred 35-day-old weaned piglets were allotted into two groups and fed either a control (C) diet or a diet containing 50 g of OMSW-LP per kg (OMSW-LP) for 40 days. Blood samples were collected at 35 and 75 days of age to assess the free radical scavenging activity (FRSA), reduced glutathione (GSH) levels, catalase activity (CAT), protein carbonyls (CARBs), and thiobarbituric acid reactive species (TBARS). The OMSW-LP diet reduced the TBARS (p = 0.049) and CARB contents (p = 0.012) and increased the levels of FRSA (p = 0.005), GSH (p = 0.040), and CAT activity (p = 0.012) in the piglets’ blood, likely due to the synergistic action of the antioxidants and bioactive compounds present in the OMSW-LP mixture. Overall, the dietary inclusion of solid-state-fermented OMSW-LP at 50 g/kg could potentially serve a bio-functional purpose since it enhanced the antioxidant blood parameters in this study, a crucial factor for the health and growth of piglets post-weaning.
Full article
Figure 1
Figure 1
<p>Effect of diet on plasma (<b>a</b>) total antioxidant capacity (TAC), (<b>b</b>) carbonyl (CARB) concentration, and (<b>c</b>) thiobarbituricacidreactive species (TBARS) concentration of piglets at 35 and 75 days of age (mean ± standard error of means). C, control (C) diet with no additions; OMSW-LP, diet with 50 g of solid-state-fermented mixture of 80% olive mill stone waste (OMSW) and 20% <span class="html-italic">Lathyrus clymenum</span> pericarps (LP) added per kg. Vertical lines represent the standard error of means. ***, statistically significant difference between diets (<span class="html-italic">p</span> < 0.001; two-tailed significance of the <span class="html-italic">t</span>-test).</p> Full article ">Figure 2
<p>Effect of diet on red blood cell (<b>a</b>) catalase (CAT) activity and (<b>b</b>) glutathione (GSH) concentration of piglets at 35 and 75 days of age (mean ± standard error of means). C, control (C) diet with no additions; OMSW-LP, diet with 50 g of solid-state-fermented mixture of 80% olive mill stone waste (OMSW) and 20% <span class="html-italic">Lathyrus clymenum</span> pericarps (LP) added per kg. ***, statistically significant difference between diets (<span class="html-italic">p</span> < 0.001; two-tailed significance of the <span class="html-italic">t</span>-test).</p> Full article ">
<p>Effect of diet on plasma (<b>a</b>) total antioxidant capacity (TAC), (<b>b</b>) carbonyl (CARB) concentration, and (<b>c</b>) thiobarbituricacidreactive species (TBARS) concentration of piglets at 35 and 75 days of age (mean ± standard error of means). C, control (C) diet with no additions; OMSW-LP, diet with 50 g of solid-state-fermented mixture of 80% olive mill stone waste (OMSW) and 20% <span class="html-italic">Lathyrus clymenum</span> pericarps (LP) added per kg. Vertical lines represent the standard error of means. ***, statistically significant difference between diets (<span class="html-italic">p</span> < 0.001; two-tailed significance of the <span class="html-italic">t</span>-test).</p> Full article ">Figure 2
<p>Effect of diet on red blood cell (<b>a</b>) catalase (CAT) activity and (<b>b</b>) glutathione (GSH) concentration of piglets at 35 and 75 days of age (mean ± standard error of means). C, control (C) diet with no additions; OMSW-LP, diet with 50 g of solid-state-fermented mixture of 80% olive mill stone waste (OMSW) and 20% <span class="html-italic">Lathyrus clymenum</span> pericarps (LP) added per kg. ***, statistically significant difference between diets (<span class="html-italic">p</span> < 0.001; two-tailed significance of the <span class="html-italic">t</span>-test).</p> Full article ">
Open AccessArticle
Catalase, Glutathione Peroxidase, and Peroxiredoxin 2 in Erythrocyte Cytosol and Membrane in Hereditary Spherocytosis, Sickle Cell Disease, and β-Thalassemia
by
Daniela Melo, Fátima Ferreira, Maria José Teles, Graça Porto, Susana Coimbra, Susana Rocha and Alice Santos-Silva
Antioxidants 2024, 13(6), 629; https://doi.org/10.3390/antiox13060629 - 22 May 2024
Abstract
Catalase (CAT), glutathione peroxidase (GPx), and peroxiredoxin 2 (Prx2) can counteract the deleterious effects of oxidative stress (OS). Their binding to the red blood cell (RBC) membrane has been reported in non-immune hemolytic anemias (NIHAs). Our aim was to evaluate the relationships between
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Catalase (CAT), glutathione peroxidase (GPx), and peroxiredoxin 2 (Prx2) can counteract the deleterious effects of oxidative stress (OS). Their binding to the red blood cell (RBC) membrane has been reported in non-immune hemolytic anemias (NIHAs). Our aim was to evaluate the relationships between CAT, GPx, and Prx2, focusing on their role at the RBC membrane, in hereditary spherocytosis (HS), sickle cell disease (SCD), β-thalassemia (β-thal), and healthy individuals. The studies were performed in plasma and in the RBC cytosol and membrane, evaluating OS biomarkers and the enzymatic activities and/or the amounts of CAT, GPx, and Prx2. The binding of the enzymes to the membrane appears to be the primary protective mechanism against oxidative membrane injuries in healthy RBCs. In HS (unsplenectomized) and β-thal, translocation from the cytosol to the membrane of CAT and Prx2, respectively, was observed, probably to counteract lipid peroxidation. RBCs from splenectomized HS patients showed the highest membrane-bound hemoglobin, CAT, and GPx amounts in the membrane. SCD patients presented the lowest amount of enzyme linkage, possibly due to structural changes induced by sickle hemoglobin. The OS-induced changes and antioxidant response were different between the studied NIHAs and may contribute to the different clinical patterns in these patients.
Full article
(This article belongs to the Special Issue Oxidative-Stress in Human Diseases—3rd Edition)
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Figure 1
Figure 1
<p>Catalase, glutathione peroxidase, and peroxiredoxin 2 amounts in the red blood cell cytosol and membrane of control, hereditary spherocytosis (unsplenectomized and splenectomized), sickle cell disease, and β-thalassemia groups. Data are presented as median (interquartile range). * <span class="html-italic">p</span> < 0.05 vs. control; <sup>a</sup> <span class="html-italic">p</span> < 0.05 vs. unsplenectomized HS; <sup>b</sup> <span class="html-italic">p</span> < 0.05 vs splenectomized HS; <sup>c</sup> <span class="html-italic">p</span> < 0.05 vs. sickle cell disease. β-thal, β-thalassemia; CAT, catalase; GPx, glutathione peroxidase; HS, hereditary spherocytosis; p.d.u., procedure defined unit; Prx2, peroxiredoxin 2; SCD, sickle cell disease; spl, splenectomized; unspl, unsplenectomized.</p> Full article ">Figure 2
<p>Correlations between oxidative stress markers and antioxidant enzymes in the red blood cell membrane for control, hereditary spherocytosis (unsplenectomized and splenectomized), sickle cell disease, and β-thalassemia groups. Spearman’s rank correlation coefficient was used to evaluate the relationships between sets of data; <span class="html-italic">p</span> < 0.05 was considered statistically significant. β-thal, β-thalassemia; Act, activity; CAT, catalase; GPx, glutathione peroxidase; HS, hereditary spherocytosis; LPO, lipid peroxidation; MBH, membrane-bound hemoglobin; ns, non-significant; p.d.u., procedure defined unit; Prx2, peroxiredoxin 2; SCD, sickle cell disease; spl, splenectomized; unspl, unsplenectomized.</p> Full article ">
<p>Catalase, glutathione peroxidase, and peroxiredoxin 2 amounts in the red blood cell cytosol and membrane of control, hereditary spherocytosis (unsplenectomized and splenectomized), sickle cell disease, and β-thalassemia groups. Data are presented as median (interquartile range). * <span class="html-italic">p</span> < 0.05 vs. control; <sup>a</sup> <span class="html-italic">p</span> < 0.05 vs. unsplenectomized HS; <sup>b</sup> <span class="html-italic">p</span> < 0.05 vs splenectomized HS; <sup>c</sup> <span class="html-italic">p</span> < 0.05 vs. sickle cell disease. β-thal, β-thalassemia; CAT, catalase; GPx, glutathione peroxidase; HS, hereditary spherocytosis; p.d.u., procedure defined unit; Prx2, peroxiredoxin 2; SCD, sickle cell disease; spl, splenectomized; unspl, unsplenectomized.</p> Full article ">Figure 2
<p>Correlations between oxidative stress markers and antioxidant enzymes in the red blood cell membrane for control, hereditary spherocytosis (unsplenectomized and splenectomized), sickle cell disease, and β-thalassemia groups. Spearman’s rank correlation coefficient was used to evaluate the relationships between sets of data; <span class="html-italic">p</span> < 0.05 was considered statistically significant. β-thal, β-thalassemia; Act, activity; CAT, catalase; GPx, glutathione peroxidase; HS, hereditary spherocytosis; LPO, lipid peroxidation; MBH, membrane-bound hemoglobin; ns, non-significant; p.d.u., procedure defined unit; Prx2, peroxiredoxin 2; SCD, sickle cell disease; spl, splenectomized; unspl, unsplenectomized.</p> Full article ">
Open AccessArticle
SVHRSP Alleviates Age-Related Cognitive Deficiency by Reducing Oxidative Stress and Neuroinflammation
by
Yingzi Wang, Zhenhua Wang, Songyu Guo, Qifa Li, Yue Kong, Aoran Sui, Jianmei Ma, Li Lu, Jie Zhao and Shao Li
Antioxidants 2024, 13(6), 628; https://doi.org/10.3390/antiox13060628 - 21 May 2024
Abstract
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Background: Our previous studies have shown that scorpion venom heat-resistant synthesized peptide (SVHRSP) induces a significant extension in lifespan and improvements in age-related physiological functions in worms. However, the mechanism underlying the potential anti-aging effects of SVHRSP in mammals remains elusive. Methods: Following
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Background: Our previous studies have shown that scorpion venom heat-resistant synthesized peptide (SVHRSP) induces a significant extension in lifespan and improvements in age-related physiological functions in worms. However, the mechanism underlying the potential anti-aging effects of SVHRSP in mammals remains elusive. Methods: Following SVHRSP treatment in senescence-accelerated mouse resistant 1 (SAMR1) or senescence-accelerated mouse prone 8 (SAMP8) mice, behavioral tests were conducted and brain tissues were collected for morphological analysis, electrophysiology experiments, flow cytometry, and protein or gene expression. The human neuroblastoma cell line (SH-SY5Y) was subjected to H2O2 treatment in cell experiments, aiming to establish a cytotoxic model that mimics cellular senescence. This model was utilized to investigate the regulatory mechanisms underlying oxidative stress and neuroinflammation associated with age-related cognitive impairment mediated by SVHRSP. Results: SVHRSP significantly ameliorated age-related cognitive decline, enhanced long-term potentiation, restored synaptic loss, and upregulated the expression of synaptic proteins, therefore indicating an improvement in synaptic plasticity. Moreover, SVHRSP demonstrated a decline in senescent markers, including SA-β-gal enzyme activity, P16, P21, SIRT1, and cell cycle arrest. The underlying mechanisms involve an upregulation of antioxidant enzyme activity and a reduction in oxidative stress-induced damage. Furthermore, SVHRSP regulated the nucleoplasmic distribution of NRF2 through the SIRT1-P53 pathway. Further investigation indicated a reduction in the expression of proinflammatory factors in the brain after SVHRSP treatment. SVHRSP attenuated neuroinflammation by regulating the NF-κB nucleoplasmic distribution and inhibiting microglial and astrocytic activation through the SIRT1-NF-κB pathway. Additionally, SVHRSP significantly augmented Nissl body count while suppressing neuronal loss. Conclusion: SVHRSP could remarkably improve cognitive deficiency by inhibiting oxidative stress and neuroinflammation, thus representing an effective strategy to improve brain health.
Full article
Figure 1
Figure 1
<p>SVHRSP reduced memory impairment and improved synaptic functions. (<b>A</b>–<b>H</b>) The effects of SVHRSP on behavioral testing. (<b>A</b>) The escape latency of the passive avoidance experiment; (<b>B</b>) the number of mice that entered the dark room in the passive avoidance test; (<b>C</b>) a device structure-style diagram of the Y Maze; (<b>D</b>) the percentage of spontaneous alternate behavior in the Y-maze trial; (<b>E</b>) the discrimination index of each group of mice in the NOR test; (<b>F</b>) the identification index of each group of mice in the NOR test; (<b>G</b>) the escape latency to reach the platform in the MWM training phase; (<b>H</b>) the number of mice crossing the platform in the MWM probe trials; (<b>I</b>,<b>J</b>) The effects of SVHRSP on long-term potentiation including slope change and amplitude change; (<b>K</b>) The effects of SVHRSP on the synaptic ultrastructure in the hippocampus; The red arrows indicate the presence of synaptic vesicles and postsynaptic dense bodies. (<b>L</b>–<b>N</b>) the representative Western blot bands and the quantification of relative protein expression for SYN and PSD95. The bars represent the mean ± SD. * <span class="html-italic">p</span> < 0.05, ** <span class="html-italic">p</span> < 0.01, <sup>#</sup> <span class="html-italic">p</span> < 0.05, versus the indicated groups.</p> Full article ">Figure 2
<p>SVHRSP downregulated the expression of aging markers. (<b>A</b>,<b>B</b>) Representative SA-β-gal staining images and quantitative analysis in SAMP8 mice. (<b>C</b>) Representative WB bands. (<b>D</b>,<b>E</b>) Quantitative analysis of P21 and P16 in vivo. (<b>F</b>–<b>H</b>) Quantitative analysis of GSH-PX, SOD, and MDA enzyme activity in vivo. (<b>I</b>,<b>J</b>) Representative SA-β-gal staining images and quantitative analysis in H<sub>2</sub>O<sub>2</sub>-induced SH-SY5Y cells. (<b>K</b>) Representative WB bands. (<b>L</b>,<b>M</b>) Quantitative analysis of P21 and p1 in vitro. (<b>N</b>,<b>O</b>) Quantitative analysis of cell cycle arrest in the G0/G1 phase. The cell fraction in the G0/G1 phase, G2/M phase, and S phase was calculated. The bars represent the mean ± SD. * <span class="html-italic">p</span> < 0.05, ** <span class="html-italic">p</span> < 0.01, *** <span class="html-italic">p</span> < 0.001, <sup>#</sup> <span class="html-italic">p</span> < 0.05, versus the indicated groups (<span class="html-italic">n</span> = 3 for each group).</p> Full article ">Figure 3
<p>SVHRSP can inhibit the SIRT1/P53 signaling pathway, leading to enhanced nuclear translocation of NRF-2 and subsequently promoting the expression of antioxidants in SAMP8 mice. (<b>A</b>) Representative WB bands. (<b>B</b>,<b>C</b>) Quantitative analysis of SIRT1 and P53 in vivo. (<b>D</b>) Representative WB bands. (<b>E</b>,<b>F</b>) Quantitative analysis of SIRT1 and P53 in vitro. (<b>G</b>–<b>J</b>) Representative WB bands and quantification analysis of nuclear NRF2 and cytoplasmic NRF2. (<b>K</b>,<b>L</b>) Immunofluorescence images and quantification analysis of NRF2 cells/total cells (scale bar = 10 μm). (<b>M</b>) Representative WB bands. (<b>N</b>,<b>O</b>) Quantitative analysis of SOD 1 and HO-1 in vivo. (<b>P</b>–<b>R</b>) mRNA quantitative analysis of <span class="html-italic">SOD 1</span>, <span class="html-italic">Hmox-1,</span> and <span class="html-italic">NQO1</span> in vivo. (<b>S</b>–<b>W</b>) Representative WB bands and quantitative analysis of SOD 1, HO-1, and NQO 1 in vitro. The bars represent the mean ± SD. ns = not significant, * <span class="html-italic">p</span> < 0.05, ** <span class="html-italic">p</span> < 0.01, *** <span class="html-italic">p</span> < 0.001 versus the indicated groups (<span class="html-italic">n</span> = 3 for each group).</p> Full article ">Figure 4
<p>SVHRSP exerts inhibitory effects on neuroinflammation in SAMP8 mice by modulating the MAPKs/NF-κB signaling pathway. (<b>A</b>–<b>D</b>) Representative Western blot bands and quantitative analysis of cytoplasmic NF-κB p65 and nuclear NF-κB p65. (<b>E</b>–<b>H</b>) Representative Western blot bands and quantification analysis of p-JNK, JNK, p-P38, and P38. (<b>I</b>–<b>K</b>) Quantitative analysis of the serum level of <span class="html-italic">IL-1B</span>, <span class="html-italic">IL-6,</span> and <span class="html-italic">TNF-α</span> measured by using ELISA. (<b>L</b>–<b>N</b>) Quantitative analysis of the mRNA level of <span class="html-italic">IL-1B</span>, <span class="html-italic">IL-6,</span> and <span class="html-italic">TNF-α</span> measured by using QRT-PCR. (<b>O</b>) Representative immunohistochemical images of Iba-1 (left) and GFAP (right). (<b>P</b>,<b>Q</b>) Representative image and quantitative analysis of Nissl staining. The bars represent the mean ± SD. ns = not significant, * <span class="html-italic">p</span> < 0.05, ** <span class="html-italic">p</span> < 0.01, *** <span class="html-italic">p</span> < 0.001, **** <span class="html-italic">p</span> < 0.0001 versus the indicated groups. Scale bar = 50 μm (<span class="html-italic">n</span> = 3 for each group).</p> Full article ">Figure 5
<p>SVHRSP alleviates age-related cognitive deficiency by reducing oxidative stress and neuroinflammation. SVHRSP can enhance the expression of the SIRT1 protein, reduce P53 activity, promote the nuclear translocation of the NRF2 transcription factor, and induce the expression of antioxidant enzymes such as SOD1, NQO1, and HO-1 to counteract oxidative stress. Furthermore, SVHRSP inhibits the expression of senescence markers P16 and P21 proteins. Additionally, by suppressing NF-κB pathway activation, SVHRSP suppresses the release of inflammatory factors IL-1β, TNF-α, and IL-6. (The graphical abstract is depicted by Figdraw 2.0.)</p> Full article ">
<p>SVHRSP reduced memory impairment and improved synaptic functions. (<b>A</b>–<b>H</b>) The effects of SVHRSP on behavioral testing. (<b>A</b>) The escape latency of the passive avoidance experiment; (<b>B</b>) the number of mice that entered the dark room in the passive avoidance test; (<b>C</b>) a device structure-style diagram of the Y Maze; (<b>D</b>) the percentage of spontaneous alternate behavior in the Y-maze trial; (<b>E</b>) the discrimination index of each group of mice in the NOR test; (<b>F</b>) the identification index of each group of mice in the NOR test; (<b>G</b>) the escape latency to reach the platform in the MWM training phase; (<b>H</b>) the number of mice crossing the platform in the MWM probe trials; (<b>I</b>,<b>J</b>) The effects of SVHRSP on long-term potentiation including slope change and amplitude change; (<b>K</b>) The effects of SVHRSP on the synaptic ultrastructure in the hippocampus; The red arrows indicate the presence of synaptic vesicles and postsynaptic dense bodies. (<b>L</b>–<b>N</b>) the representative Western blot bands and the quantification of relative protein expression for SYN and PSD95. The bars represent the mean ± SD. * <span class="html-italic">p</span> < 0.05, ** <span class="html-italic">p</span> < 0.01, <sup>#</sup> <span class="html-italic">p</span> < 0.05, versus the indicated groups.</p> Full article ">Figure 2
<p>SVHRSP downregulated the expression of aging markers. (<b>A</b>,<b>B</b>) Representative SA-β-gal staining images and quantitative analysis in SAMP8 mice. (<b>C</b>) Representative WB bands. (<b>D</b>,<b>E</b>) Quantitative analysis of P21 and P16 in vivo. (<b>F</b>–<b>H</b>) Quantitative analysis of GSH-PX, SOD, and MDA enzyme activity in vivo. (<b>I</b>,<b>J</b>) Representative SA-β-gal staining images and quantitative analysis in H<sub>2</sub>O<sub>2</sub>-induced SH-SY5Y cells. (<b>K</b>) Representative WB bands. (<b>L</b>,<b>M</b>) Quantitative analysis of P21 and p1 in vitro. (<b>N</b>,<b>O</b>) Quantitative analysis of cell cycle arrest in the G0/G1 phase. The cell fraction in the G0/G1 phase, G2/M phase, and S phase was calculated. The bars represent the mean ± SD. * <span class="html-italic">p</span> < 0.05, ** <span class="html-italic">p</span> < 0.01, *** <span class="html-italic">p</span> < 0.001, <sup>#</sup> <span class="html-italic">p</span> < 0.05, versus the indicated groups (<span class="html-italic">n</span> = 3 for each group).</p> Full article ">Figure 3
<p>SVHRSP can inhibit the SIRT1/P53 signaling pathway, leading to enhanced nuclear translocation of NRF-2 and subsequently promoting the expression of antioxidants in SAMP8 mice. (<b>A</b>) Representative WB bands. (<b>B</b>,<b>C</b>) Quantitative analysis of SIRT1 and P53 in vivo. (<b>D</b>) Representative WB bands. (<b>E</b>,<b>F</b>) Quantitative analysis of SIRT1 and P53 in vitro. (<b>G</b>–<b>J</b>) Representative WB bands and quantification analysis of nuclear NRF2 and cytoplasmic NRF2. (<b>K</b>,<b>L</b>) Immunofluorescence images and quantification analysis of NRF2 cells/total cells (scale bar = 10 μm). (<b>M</b>) Representative WB bands. (<b>N</b>,<b>O</b>) Quantitative analysis of SOD 1 and HO-1 in vivo. (<b>P</b>–<b>R</b>) mRNA quantitative analysis of <span class="html-italic">SOD 1</span>, <span class="html-italic">Hmox-1,</span> and <span class="html-italic">NQO1</span> in vivo. (<b>S</b>–<b>W</b>) Representative WB bands and quantitative analysis of SOD 1, HO-1, and NQO 1 in vitro. The bars represent the mean ± SD. ns = not significant, * <span class="html-italic">p</span> < 0.05, ** <span class="html-italic">p</span> < 0.01, *** <span class="html-italic">p</span> < 0.001 versus the indicated groups (<span class="html-italic">n</span> = 3 for each group).</p> Full article ">Figure 4
<p>SVHRSP exerts inhibitory effects on neuroinflammation in SAMP8 mice by modulating the MAPKs/NF-κB signaling pathway. (<b>A</b>–<b>D</b>) Representative Western blot bands and quantitative analysis of cytoplasmic NF-κB p65 and nuclear NF-κB p65. (<b>E</b>–<b>H</b>) Representative Western blot bands and quantification analysis of p-JNK, JNK, p-P38, and P38. (<b>I</b>–<b>K</b>) Quantitative analysis of the serum level of <span class="html-italic">IL-1B</span>, <span class="html-italic">IL-6,</span> and <span class="html-italic">TNF-α</span> measured by using ELISA. (<b>L</b>–<b>N</b>) Quantitative analysis of the mRNA level of <span class="html-italic">IL-1B</span>, <span class="html-italic">IL-6,</span> and <span class="html-italic">TNF-α</span> measured by using QRT-PCR. (<b>O</b>) Representative immunohistochemical images of Iba-1 (left) and GFAP (right). (<b>P</b>,<b>Q</b>) Representative image and quantitative analysis of Nissl staining. The bars represent the mean ± SD. ns = not significant, * <span class="html-italic">p</span> < 0.05, ** <span class="html-italic">p</span> < 0.01, *** <span class="html-italic">p</span> < 0.001, **** <span class="html-italic">p</span> < 0.0001 versus the indicated groups. Scale bar = 50 μm (<span class="html-italic">n</span> = 3 for each group).</p> Full article ">Figure 5
<p>SVHRSP alleviates age-related cognitive deficiency by reducing oxidative stress and neuroinflammation. SVHRSP can enhance the expression of the SIRT1 protein, reduce P53 activity, promote the nuclear translocation of the NRF2 transcription factor, and induce the expression of antioxidant enzymes such as SOD1, NQO1, and HO-1 to counteract oxidative stress. Furthermore, SVHRSP inhibits the expression of senescence markers P16 and P21 proteins. Additionally, by suppressing NF-κB pathway activation, SVHRSP suppresses the release of inflammatory factors IL-1β, TNF-α, and IL-6. (The graphical abstract is depicted by Figdraw 2.0.)</p> Full article ">
Open AccessArticle
The Effect of Ovariectomy and Estradiol Substitution on the Metabolic Parameters and Transcriptomic Profile of Adipose Tissue in a Prediabetic Model
by
Irena Marková, Martina Hüttl, Denisa Miklánková, Lucie Šedová, Ondřej Šeda and Hana Malínská
Antioxidants 2024, 13(6), 627; https://doi.org/10.3390/antiox13060627 - 21 May 2024
Abstract
Menopause brings about profound physiological changes, including the acceleration of insulin resistance and other abnormalities, in which adipose tissue can play a significant role. This study analyzed the effect of ovariectomy and estradiol substitution on the metabolic parameters and transcriptomic profile of adipose
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Menopause brings about profound physiological changes, including the acceleration of insulin resistance and other abnormalities, in which adipose tissue can play a significant role. This study analyzed the effect of ovariectomy and estradiol substitution on the metabolic parameters and transcriptomic profile of adipose tissue in prediabetic females of hereditary hypertriglyceridemic rats (HHTgs). The HHTgs underwent ovariectomy (OVX) or sham surgery (SHAM), and half of the OVX group received 17β-estradiol (OVX+E2) post-surgery. Ovariectomy resulted in weight gain, an impaired glucose tolerance, ectopic triglyceride (TG) deposition, and insulin resistance exemplified by impaired glycogenesis and lipogenesis. Estradiol alleviated some of the disorders associated with ovariectomy; in particular, it improved insulin sensitivity and reduced TG deposition. A transcriptomic analysis of perimetrial adipose tissue revealed 809 differentially expressed transcripts in the OVX vs. SHAM groups, mostly pertaining to the regulation of lipid and glucose metabolism, and oxidative stress. Estradiol substitution affected 1049 transcripts with overrepresentation in the signaling pathways of lipid metabolism. The principal component and hierarchical clustering analyses of transcriptome shifts corroborated the metabolic data, showing a closer resemblance between the OVX+E2 and SHAM groups compared to the OVX group. Changes in the adipose tissue transcriptome may contribute to metabolic abnormalities accompanying ovariectomy-induced menopause in HHTg females. Estradiol substitution may partially mitigate some of these disorders.
Full article
Open AccessArticle
AQP3 and AQP5 Modulation in Response to Prolonged Oxidative Stress in Breast Cancer Cell Lines
by
Monika Mlinarić, Ivan Lučić, Marko Tomljanović, Ivana Tartaro Bujak, Lidija Milković and Ana Čipak Gašparović
Antioxidants 2024, 13(6), 626; https://doi.org/10.3390/antiox13060626 - 21 May 2024
Abstract
Aquaporins are membrane pores regulating the transport of water, glycerol, and other small molecules across membranes. Among 13 human aquaporins, six have been shown to transport H2O2 and are therefore called peroxiporins. Peroxiporins are implicated in cancer development and progression,
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Aquaporins are membrane pores regulating the transport of water, glycerol, and other small molecules across membranes. Among 13 human aquaporins, six have been shown to transport H2O2 and are therefore called peroxiporins. Peroxiporins are implicated in cancer development and progression, partly due to their involvement in H2O2 transport. Oxidative stress is linked to breast cancer development but is also a mechanism of action for conventional chemotherapy. The aim of this study is to investigate the effects of prolonged oxidative stress on Aquaporin 3 (AQP3), Aquaporin 5 (AQP5), and signaling pathways in breast cancer cell lines of different malignancies alongside a non-tumorigenic breast cell line. The prolonged oxidative stress caused responses in viability only in the cancer cell lines, while it affected cell migration in the MCF7 cell line. Changes in the localization of NRF2, a transcription factor involved in oxidative stress response, were observed only in the cancer cell lines, and no effects were recorded on its downstream target proteins. Moreover, the prolonged oxidative stress caused changes in AQP3 and AQP5 expression only in the cancer cell lines, in contrast to their non-malignant counterparts. These results suggest peroxiporins are potential therapeutic targets in cancer treatment. However, further research is needed to elucidate their role in the modulation of therapy response, highlighting the importance of research on this topic.
Full article
(This article belongs to the Special Issue Oxidative Stress and NRF2 in Health and Disease)
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Figure 1
Figure 1
<p>Effect of prolonged exposure to H<sub>2</sub>O<sub>2</sub> on cell viability and proliferation. Cells were treated with 10 or 20 µM H<sub>2</sub>O<sub>2</sub> for 14 days, after which they were treated with a range of H<sub>2</sub>O<sub>2</sub> concentrations. After 24 h, cell viability and proliferation were assessed by MTT and BrdU assays. Cell viability is shown on panels (<b>a</b>) SUM159PT, (<b>b</b>) SkBr3, (<b>c</b>) MCF7, and (<b>d</b>) MCF10A. Cell proliferation is shown on panels (<b>e</b>) SUM159PT, (<b>f</b>) SkBr3, (<b>g</b>) MCF7, and (<b>h</b>) MCF10A. Experiments were performed biologically and technically in triplicate. Cell viability was calculated as the ratio between the treated cells and untreated control and is shown as a percentage of the control. The results are presented as mean ± SEM. The asterisk (*) indicates the <span class="html-italic">p</span> value for the 10 µM-treated cells compared to the control, and the plus (<sup>+</sup>) indicates the <span class="html-italic">p</span> value for the 20 µM H<sub>2</sub>O<sub>2</sub>-treated cells compared to the control, *<sup>/+</sup> <span class="html-italic">p</span> ≤ 0.05, **<sup>/++</sup> <span class="html-italic">p</span> ≤ 0.01, ***<sup>/+++</sup> <span class="html-italic">p</span> ≤ 0.001, ****<sup>/++++</sup> <span class="html-italic">p</span> ≤ 0.0001.</p> Full article ">Figure 2
<p>Effect of prolonged exposure to H<sub>2</sub>O<sub>2</sub> on cell migration. (<b>a</b>) SUM159PT, (<b>b</b>) SkBr3, (<b>c</b>) MCF7, and (<b>d</b>) MCF10A cell lines were treated with 20 µM H<sub>2</sub>O<sub>2</sub> for 14 days, after which they were scratched and treated with 20 µM H<sub>2</sub>O<sub>2</sub>. Cells were photographed after scratching as well as 24 and 48 h afterwards. Cell migration is calculated as the reduction in wound area over time, shown as a percentage of the starting wound area. Experiments were performed biologically and technically in triplicate. Results are presented as mean ± SEM. * <span class="html-italic">p</span> ≤ 0.05 compared to untreated control; <sup>+++</sup> <span class="html-italic">p</span> ≤ 0.001 compared to 20 µM H<sub>2</sub>O<sub>2</sub>-treated cells.</p> Full article ">Figure 3
<p>Effect of prolonged exposure to H<sub>2</sub>O<sub>2</sub> on fatty acid content and lipid hydroperoxide (LOOH) formation. Cells were treated with 20 µM H<sub>2</sub>O<sub>2</sub> for 14 days, after which cells were collected for analysis. The effect of H<sub>2</sub>O<sub>2</sub> on lipid composition is shown in panels (<b>a</b>) SUM159PT, (<b>b</b>) SkBr3, (<b>c</b>) MCF7, and (<b>d</b>) MCF10A, and the effect on lipid hydroperoxide formation is shown in panels (<b>e</b>) SUM159PT, (<b>f</b>) SkBr3, (<b>g</b>) MCF7, and (<b>h</b>) MCF10A. Experiments were performed biologically and technically in triplicate. Results are presented as mean ± SEM.</p> Full article ">Figure 4
<p>Effect of prolonged exposure to H<sub>2</sub>O<sub>2</sub> on protein and gene expression. Cells were treated with 20 µM H<sub>2</sub>O<sub>2</sub> for 14 days, after which proteins were harvested and assayed by Western blotting, and total RNA was isolated, transcribed into cDNA, and analyzed by RT-qPCR. NRF2, Keap1, GSK3β, HO-1, NQO1, and AKR1B10 protein expressions were analyzed in (<b>a</b>) SUM159PT, (<b>b</b>) SkBr3, (<b>c</b>) MCF7, and (<b>d</b>) MCF10A. After the same treatment, cytoplasmatic and nuclear protein fractions were isolated and assayed by Western blotting, and (<b>f</b>) NRF2 protein localization was analyzed. Protein level is shown as a relative value compared to untreated control. Representative immunoreactive bands are shown in panels (<b>e</b>,<b>h</b>). <span class="html-italic">NFE2L2</span> gene expression is shown in panel (<b>g</b>). Expression fold change in a target gene is shown compared to untreated control. Experiments were performed biologically and technically in triplicate. Results are presented as mean ± SEM. * <span class="html-italic">p</span> ≤ 0.05, ** <span class="html-italic">p</span> ≤ 0.01, and **** <span class="html-italic">p</span> ≤ 0.0001 compared to untreated control.</p> Full article ">Figure 5
<p>Effect of prolonged exposure to H<sub>2</sub>O<sub>2</sub> on PI3K, PTEN, pAkt, Akt, Raptor, Rictor, p-mTOR, and Ras protein expression. (<b>a</b>) SUM159PT, (<b>b</b>) SkBr3, (<b>c</b>) MCF7, and (<b>d</b>) MCF10A cell lines were treated with 20 µM H<sub>2</sub>O<sub>2</sub> for 14 days, after which proteins were harvested and assayed by Western blotting. Protein level is shown as a relative value compared to untreated control, and pAkt/Akt is shown as a ratio. Experiments were performed biologically and technically in triplicate. Results are presented as mean ± SEM. * <span class="html-italic">p</span> ≤ 0.05 compared to untreated control.</p> Full article ">Figure 6
<p>Effect of prolonged exposure to H<sub>2</sub>O<sub>2</sub> on protein and gene expression. Cells were treated with 20 µM H<sub>2</sub>O<sub>2</sub> for 14 days, after which proteins were harvested and assayed by Western blotting, and total RNA was isolated, transcribed into cDNA, and analyzed by RT-qPCR. ABCB1 and ABCG2 protein expressions were analyzed in (<b>a</b>) SUM159PT, (<b>b</b>) SkBr3, (<b>c</b>) MCF7, and (<b>d</b>) MCF10A, and AQP3 and AQP5 protein expressions in (<b>e</b>) SUM159PT, (<b>f</b>) SkBr3, (<b>g</b>) MCF7, and (<b>h</b>) MCF10A. Protein level is shown as a relative value compared to untreated control. Representative immunoreactive bands are shown in panel (<b>i</b>). <span class="html-italic">AQP1</span>, <span class="html-italic">AQP3</span>, <span class="html-italic">AQP5</span>, <span class="html-italic">AQP9</span>, and <span class="html-italic">AQP11</span> gene expressions were analyzed in (<b>j</b>) SUM159PT, (<b>k</b>) SkBr3, (<b>l</b>) MCF7, and (<b>m</b>) MCF10A. Expression fold change in a target gene is shown compared to untreated control. Experiments were performed biologically and technically in triplicate. Results are presented as mean ± SEM. * <span class="html-italic">p</span> ≤ 0.05, ** <span class="html-italic">p</span> ≤ 0.01, and *** <span class="html-italic">p</span> ≤ 0.001 compared to untreated control.</p> Full article ">
<p>Effect of prolonged exposure to H<sub>2</sub>O<sub>2</sub> on cell viability and proliferation. Cells were treated with 10 or 20 µM H<sub>2</sub>O<sub>2</sub> for 14 days, after which they were treated with a range of H<sub>2</sub>O<sub>2</sub> concentrations. After 24 h, cell viability and proliferation were assessed by MTT and BrdU assays. Cell viability is shown on panels (<b>a</b>) SUM159PT, (<b>b</b>) SkBr3, (<b>c</b>) MCF7, and (<b>d</b>) MCF10A. Cell proliferation is shown on panels (<b>e</b>) SUM159PT, (<b>f</b>) SkBr3, (<b>g</b>) MCF7, and (<b>h</b>) MCF10A. Experiments were performed biologically and technically in triplicate. Cell viability was calculated as the ratio between the treated cells and untreated control and is shown as a percentage of the control. The results are presented as mean ± SEM. The asterisk (*) indicates the <span class="html-italic">p</span> value for the 10 µM-treated cells compared to the control, and the plus (<sup>+</sup>) indicates the <span class="html-italic">p</span> value for the 20 µM H<sub>2</sub>O<sub>2</sub>-treated cells compared to the control, *<sup>/+</sup> <span class="html-italic">p</span> ≤ 0.05, **<sup>/++</sup> <span class="html-italic">p</span> ≤ 0.01, ***<sup>/+++</sup> <span class="html-italic">p</span> ≤ 0.001, ****<sup>/++++</sup> <span class="html-italic">p</span> ≤ 0.0001.</p> Full article ">Figure 2
<p>Effect of prolonged exposure to H<sub>2</sub>O<sub>2</sub> on cell migration. (<b>a</b>) SUM159PT, (<b>b</b>) SkBr3, (<b>c</b>) MCF7, and (<b>d</b>) MCF10A cell lines were treated with 20 µM H<sub>2</sub>O<sub>2</sub> for 14 days, after which they were scratched and treated with 20 µM H<sub>2</sub>O<sub>2</sub>. Cells were photographed after scratching as well as 24 and 48 h afterwards. Cell migration is calculated as the reduction in wound area over time, shown as a percentage of the starting wound area. Experiments were performed biologically and technically in triplicate. Results are presented as mean ± SEM. * <span class="html-italic">p</span> ≤ 0.05 compared to untreated control; <sup>+++</sup> <span class="html-italic">p</span> ≤ 0.001 compared to 20 µM H<sub>2</sub>O<sub>2</sub>-treated cells.</p> Full article ">Figure 3
<p>Effect of prolonged exposure to H<sub>2</sub>O<sub>2</sub> on fatty acid content and lipid hydroperoxide (LOOH) formation. Cells were treated with 20 µM H<sub>2</sub>O<sub>2</sub> for 14 days, after which cells were collected for analysis. The effect of H<sub>2</sub>O<sub>2</sub> on lipid composition is shown in panels (<b>a</b>) SUM159PT, (<b>b</b>) SkBr3, (<b>c</b>) MCF7, and (<b>d</b>) MCF10A, and the effect on lipid hydroperoxide formation is shown in panels (<b>e</b>) SUM159PT, (<b>f</b>) SkBr3, (<b>g</b>) MCF7, and (<b>h</b>) MCF10A. Experiments were performed biologically and technically in triplicate. Results are presented as mean ± SEM.</p> Full article ">Figure 4
<p>Effect of prolonged exposure to H<sub>2</sub>O<sub>2</sub> on protein and gene expression. Cells were treated with 20 µM H<sub>2</sub>O<sub>2</sub> for 14 days, after which proteins were harvested and assayed by Western blotting, and total RNA was isolated, transcribed into cDNA, and analyzed by RT-qPCR. NRF2, Keap1, GSK3β, HO-1, NQO1, and AKR1B10 protein expressions were analyzed in (<b>a</b>) SUM159PT, (<b>b</b>) SkBr3, (<b>c</b>) MCF7, and (<b>d</b>) MCF10A. After the same treatment, cytoplasmatic and nuclear protein fractions were isolated and assayed by Western blotting, and (<b>f</b>) NRF2 protein localization was analyzed. Protein level is shown as a relative value compared to untreated control. Representative immunoreactive bands are shown in panels (<b>e</b>,<b>h</b>). <span class="html-italic">NFE2L2</span> gene expression is shown in panel (<b>g</b>). Expression fold change in a target gene is shown compared to untreated control. Experiments were performed biologically and technically in triplicate. Results are presented as mean ± SEM. * <span class="html-italic">p</span> ≤ 0.05, ** <span class="html-italic">p</span> ≤ 0.01, and **** <span class="html-italic">p</span> ≤ 0.0001 compared to untreated control.</p> Full article ">Figure 5
<p>Effect of prolonged exposure to H<sub>2</sub>O<sub>2</sub> on PI3K, PTEN, pAkt, Akt, Raptor, Rictor, p-mTOR, and Ras protein expression. (<b>a</b>) SUM159PT, (<b>b</b>) SkBr3, (<b>c</b>) MCF7, and (<b>d</b>) MCF10A cell lines were treated with 20 µM H<sub>2</sub>O<sub>2</sub> for 14 days, after which proteins were harvested and assayed by Western blotting. Protein level is shown as a relative value compared to untreated control, and pAkt/Akt is shown as a ratio. Experiments were performed biologically and technically in triplicate. Results are presented as mean ± SEM. * <span class="html-italic">p</span> ≤ 0.05 compared to untreated control.</p> Full article ">Figure 6
<p>Effect of prolonged exposure to H<sub>2</sub>O<sub>2</sub> on protein and gene expression. Cells were treated with 20 µM H<sub>2</sub>O<sub>2</sub> for 14 days, after which proteins were harvested and assayed by Western blotting, and total RNA was isolated, transcribed into cDNA, and analyzed by RT-qPCR. ABCB1 and ABCG2 protein expressions were analyzed in (<b>a</b>) SUM159PT, (<b>b</b>) SkBr3, (<b>c</b>) MCF7, and (<b>d</b>) MCF10A, and AQP3 and AQP5 protein expressions in (<b>e</b>) SUM159PT, (<b>f</b>) SkBr3, (<b>g</b>) MCF7, and (<b>h</b>) MCF10A. Protein level is shown as a relative value compared to untreated control. Representative immunoreactive bands are shown in panel (<b>i</b>). <span class="html-italic">AQP1</span>, <span class="html-italic">AQP3</span>, <span class="html-italic">AQP5</span>, <span class="html-italic">AQP9</span>, and <span class="html-italic">AQP11</span> gene expressions were analyzed in (<b>j</b>) SUM159PT, (<b>k</b>) SkBr3, (<b>l</b>) MCF7, and (<b>m</b>) MCF10A. Expression fold change in a target gene is shown compared to untreated control. Experiments were performed biologically and technically in triplicate. Results are presented as mean ± SEM. * <span class="html-italic">p</span> ≤ 0.05, ** <span class="html-italic">p</span> ≤ 0.01, and *** <span class="html-italic">p</span> ≤ 0.001 compared to untreated control.</p> Full article ">
Open AccessArticle
Resveratrol-Enriched Rice Callus Extract Inhibits Oxidative and Cellular Melanogenic Activities in Melan-A Cells
by
Chaiwat Monmai, Jin-Suk Kim and So-Hyeon Baek
Antioxidants 2024, 13(6), 625; https://doi.org/10.3390/antiox13060625 - 21 May 2024
Abstract
The excessive production of melanin can cause skin diseases and hyperpigmentation. In this study, resveratrol contained in Dongjin rice seed (DJ526) was increased through callus induction. The antioxidant capacity of resveratrol-enriched rice callus was evaluated using the ABTS radical scavenging method and was
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The excessive production of melanin can cause skin diseases and hyperpigmentation. In this study, resveratrol contained in Dongjin rice seed (DJ526) was increased through callus induction. The antioxidant capacity of resveratrol-enriched rice callus was evaluated using the ABTS radical scavenging method and was equivalent to that of vitamin C. DJ526 rice callus extract significantly increased antioxidant activities in a concentration-dependent manner. The anti-melanogenesis effects of DJ526 rice callus extract were also evaluated in melan-a cells. Resveratrol-enriched rice callus extract significantly (i) decreased the size and number of melanin-containing cells, (ii) suppressed the activity of cellular tyrosinase and melanin content, (iii) downregulated the expression of microphthalmia-associated transcription factor, tyrosinase, tyrosinase-related protein-1, and tyrosinase-related protein-2, (iv) increased the expression of phosphorylated extracellular signal-regulated kinase 1/2 and protein kinase B, and (v) inhibited the activation of phosphorylated p38 in melan-a cells. From the above observations, DJ526 rice callus extract showed strong antioxidant and anti-melanogenesis activity at the concentration test. These findings indicate the potential of resveratrol-enriched rice callus as a novel agent for controlling hyperpigmentation.
Full article
(This article belongs to the Special Issue Antioxidant Capacity of Natural Products)
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Graphical abstract
Graphical abstract
Full article ">Figure 1
<p>Pearson’s correlation analysis between the amount of resveratrol (piceid + resveratrol) and scavenging activity (degrees of freedom = 22, <span class="html-italic">p</span> = 0.05).</p> Full article ">Figure 2
<p>Effect of DJ526 rice callus extract on melan-a cell viability. The concentration of DMSO and arbutin was 0.1% (<span class="html-italic">v</span>/<span class="html-italic">v</span>) and 100 µg/mL, respectively. Data are shown as mean ± standard deviation (n = 3). Significant differences at <span class="html-italic">p</span> < 0.05 when compared with medium group.</p> Full article ">Figure 3
<p>Effect of DJ526 rice callus extract on (<b>a</b>,<b>b</b>) melanin content, (<b>c</b>) Pearson’s correlation analysis between the amount of resveratrol (piceid + resveratrol) and melanin content (degrees of freedom = 22, <span class="html-italic">p</span> = 0.05), (<b>d</b>) representative L-DOPA staining at 100 µg/mL of treatments (scale bar = 50 µm), (<b>e</b>) cellular tyrosinase activity, and (<b>f</b>) Pearson’s correlation analysis between the amount of resveratrol (piceid + resveratrol) and cellular tyrosinase activity (degrees of freedom = 22, <span class="html-italic">p</span> = 0.05). The concentration of DMSO and arbutin was 0.1% (<span class="html-italic">v</span>/<span class="html-italic">v</span>) and 100 µg/mL, respectively. Data are presented as mean ± standard deviation (n = 3). Significant differences at <span class="html-italic">p</span> < 0.05. Lowercase letters (a–h) indicate significant differences at <span class="html-italic">p</span> < 0.05 among all treatments. In the statistical analysis, “a” represents the reference group, “b” represents significantly lower than the “a” group (<span class="html-italic">p</span> < 0.05), and “c” represents significantly lower than the “b” group (<span class="html-italic">p</span> < 0.05). Red arrows represent the melanin-containing cells.</p> Full article ">Figure 4
<p>Effect of DJ526 rice callus extract on (<b>a</b>) melanin-containing cells (scale bar = 50 µm), (<b>b</b>) morphological appearance of melan-a cells, (<b>c</b>) Pearson’s correlation analysis between the amount of resveratrol (piceid + resveratrol) and melanin-containing cells (degrees of freedom = 10, <span class="html-italic">p</span> = 0.05), and (<b>d</b>) Pearson’s correlation analysis between the amount of resveratrol (piceid + resveratrol) and differentiated melan-a cells scored 4+ (Δ) and 1+ (•) (degrees of freedom = 10, <span class="html-italic">p</span> = 0.05). The concentration of arbutin, DJ, and DJ526 rice callus extracts was 100 µg/mL. The concentration of DMSO was 0.1% (<span class="html-italic">v</span>/<span class="html-italic">v</span>). Lowercase letters (a–d) indicate significant differences at <span class="html-italic">p</span> < 0.05 among treatments. In the statistical analysis, “a” represents the reference group, “b” represents significantly lower than the “a” group (<span class="html-italic">p</span> < 0.05), “c” represents significantly lower than the “b” group (<span class="html-italic">p</span> < 0.05), and “d” represents significantly lower than the “c” group (<span class="html-italic">p</span> < 0.05).</p> Full article ">Figure 5
<p>Effect of DJ526 rice callus extract on melanogenesis-associated gene expression. Expression levels of (<b>a</b>) <span class="html-italic">MITF</span>, (<b>b</b>) <span class="html-italic">TRP-1</span>, (<b>c</b>) <span class="html-italic">TRP-2</span>, and (<b>d</b>) <span class="html-italic">tyrosinase</span>. Pearson’s correlation analyses between the amount of resveratrol (piceid + resveratrol) and (<b>e</b>) <span class="html-italic">MITF</span>, (<b>f</b>) <span class="html-italic">TRP-1</span>, (<b>g</b>) <span class="html-italic">TRP-2</span>, and (<b>h</b>) <span class="html-italic">tyrosinase</span> expression levels. The concentration of DMSO and arbutin was 0.1% (<span class="html-italic">v</span>/<span class="html-italic">v</span>) and 100 µg/mL, respectively. Data are shown as mean ± standard deviation. Pearson’s correlation analyses were performed with degrees of freedom = 10 and <span class="html-italic">p</span> = 0.05. Significant differences at <span class="html-italic">p</span> < 0.05. Lowercase letters (a–i) indicate significant differences at <span class="html-italic">p</span> < 0.05 among all treatments. In the statistical analysis, “a” represents the reference group, “b” represents significantly lower than the “a” group (<span class="html-italic">p</span> < 0.05), “c” represents significantly lower than the “b” group (p < 0.05), “d” represents significantly lower than the “c” group (<span class="html-italic">p</span> < 0.05), “e” represents significantly lower than the “d” group (<span class="html-italic">p</span> < 0.05), “f” represents significantly lower than the “e” group (<span class="html-italic">p</span> < 0.05), “g” represents significantly lower than the “f” group (<span class="html-italic">p</span> < 0.05), “h” represents significantly lower than the “g” group (<span class="html-italic">p</span> < 0.05), and “i” represents significantly lower than the “h” group (<span class="html-italic">p</span> < 0.05).</p> Full article ">Figure 6
<p>Effect of DJ526 rice callus extract on (<b>a</b>) melanogenesis-related protein expression and (<b>b</b>) inflammatory-related protein expression. Data are presented as mean ± standard deviation. Significant differences at <span class="html-italic">p</span> < 0.05. Lowercase letters (a–d) indicate significant differences at <span class="html-italic">p</span> < 0.05 among the treatments. In the statistical analysis, “a” represents the reference group, “b” represents significantly lower than the “a” group (<span class="html-italic">p</span> < 0.05), “c” represents significantly lower than the “b” group (<span class="html-italic">p</span> < 0.05), and “d” represents significantly lower than the “c” group (<span class="html-italic">p</span> < 0.05).</p> Full article ">
Full article ">Figure 1
<p>Pearson’s correlation analysis between the amount of resveratrol (piceid + resveratrol) and scavenging activity (degrees of freedom = 22, <span class="html-italic">p</span> = 0.05).</p> Full article ">Figure 2
<p>Effect of DJ526 rice callus extract on melan-a cell viability. The concentration of DMSO and arbutin was 0.1% (<span class="html-italic">v</span>/<span class="html-italic">v</span>) and 100 µg/mL, respectively. Data are shown as mean ± standard deviation (n = 3). Significant differences at <span class="html-italic">p</span> < 0.05 when compared with medium group.</p> Full article ">Figure 3
<p>Effect of DJ526 rice callus extract on (<b>a</b>,<b>b</b>) melanin content, (<b>c</b>) Pearson’s correlation analysis between the amount of resveratrol (piceid + resveratrol) and melanin content (degrees of freedom = 22, <span class="html-italic">p</span> = 0.05), (<b>d</b>) representative L-DOPA staining at 100 µg/mL of treatments (scale bar = 50 µm), (<b>e</b>) cellular tyrosinase activity, and (<b>f</b>) Pearson’s correlation analysis between the amount of resveratrol (piceid + resveratrol) and cellular tyrosinase activity (degrees of freedom = 22, <span class="html-italic">p</span> = 0.05). The concentration of DMSO and arbutin was 0.1% (<span class="html-italic">v</span>/<span class="html-italic">v</span>) and 100 µg/mL, respectively. Data are presented as mean ± standard deviation (n = 3). Significant differences at <span class="html-italic">p</span> < 0.05. Lowercase letters (a–h) indicate significant differences at <span class="html-italic">p</span> < 0.05 among all treatments. In the statistical analysis, “a” represents the reference group, “b” represents significantly lower than the “a” group (<span class="html-italic">p</span> < 0.05), and “c” represents significantly lower than the “b” group (<span class="html-italic">p</span> < 0.05). Red arrows represent the melanin-containing cells.</p> Full article ">Figure 4
<p>Effect of DJ526 rice callus extract on (<b>a</b>) melanin-containing cells (scale bar = 50 µm), (<b>b</b>) morphological appearance of melan-a cells, (<b>c</b>) Pearson’s correlation analysis between the amount of resveratrol (piceid + resveratrol) and melanin-containing cells (degrees of freedom = 10, <span class="html-italic">p</span> = 0.05), and (<b>d</b>) Pearson’s correlation analysis between the amount of resveratrol (piceid + resveratrol) and differentiated melan-a cells scored 4+ (Δ) and 1+ (•) (degrees of freedom = 10, <span class="html-italic">p</span> = 0.05). The concentration of arbutin, DJ, and DJ526 rice callus extracts was 100 µg/mL. The concentration of DMSO was 0.1% (<span class="html-italic">v</span>/<span class="html-italic">v</span>). Lowercase letters (a–d) indicate significant differences at <span class="html-italic">p</span> < 0.05 among treatments. In the statistical analysis, “a” represents the reference group, “b” represents significantly lower than the “a” group (<span class="html-italic">p</span> < 0.05), “c” represents significantly lower than the “b” group (<span class="html-italic">p</span> < 0.05), and “d” represents significantly lower than the “c” group (<span class="html-italic">p</span> < 0.05).</p> Full article ">Figure 5
<p>Effect of DJ526 rice callus extract on melanogenesis-associated gene expression. Expression levels of (<b>a</b>) <span class="html-italic">MITF</span>, (<b>b</b>) <span class="html-italic">TRP-1</span>, (<b>c</b>) <span class="html-italic">TRP-2</span>, and (<b>d</b>) <span class="html-italic">tyrosinase</span>. Pearson’s correlation analyses between the amount of resveratrol (piceid + resveratrol) and (<b>e</b>) <span class="html-italic">MITF</span>, (<b>f</b>) <span class="html-italic">TRP-1</span>, (<b>g</b>) <span class="html-italic">TRP-2</span>, and (<b>h</b>) <span class="html-italic">tyrosinase</span> expression levels. The concentration of DMSO and arbutin was 0.1% (<span class="html-italic">v</span>/<span class="html-italic">v</span>) and 100 µg/mL, respectively. Data are shown as mean ± standard deviation. Pearson’s correlation analyses were performed with degrees of freedom = 10 and <span class="html-italic">p</span> = 0.05. Significant differences at <span class="html-italic">p</span> < 0.05. Lowercase letters (a–i) indicate significant differences at <span class="html-italic">p</span> < 0.05 among all treatments. In the statistical analysis, “a” represents the reference group, “b” represents significantly lower than the “a” group (<span class="html-italic">p</span> < 0.05), “c” represents significantly lower than the “b” group (p < 0.05), “d” represents significantly lower than the “c” group (<span class="html-italic">p</span> < 0.05), “e” represents significantly lower than the “d” group (<span class="html-italic">p</span> < 0.05), “f” represents significantly lower than the “e” group (<span class="html-italic">p</span> < 0.05), “g” represents significantly lower than the “f” group (<span class="html-italic">p</span> < 0.05), “h” represents significantly lower than the “g” group (<span class="html-italic">p</span> < 0.05), and “i” represents significantly lower than the “h” group (<span class="html-italic">p</span> < 0.05).</p> Full article ">Figure 6
<p>Effect of DJ526 rice callus extract on (<b>a</b>) melanogenesis-related protein expression and (<b>b</b>) inflammatory-related protein expression. Data are presented as mean ± standard deviation. Significant differences at <span class="html-italic">p</span> < 0.05. Lowercase letters (a–d) indicate significant differences at <span class="html-italic">p</span> < 0.05 among the treatments. In the statistical analysis, “a” represents the reference group, “b” represents significantly lower than the “a” group (<span class="html-italic">p</span> < 0.05), “c” represents significantly lower than the “b” group (<span class="html-italic">p</span> < 0.05), and “d” represents significantly lower than the “c” group (<span class="html-italic">p</span> < 0.05).</p> Full article ">
Open AccessReview
Advancements in Understanding and Enhancing Antioxidant-Mediated Sperm Cryopreservation in Small Ruminants: Challenges and Perspectives
by
Daniel Ionut Berean, Liviu Marian Bogdan and Raluca Cimpean
Antioxidants 2024, 13(6), 624; https://doi.org/10.3390/antiox13060624 - 21 May 2024
Abstract
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Cryopreservation poses significant challenges to the preservation of sperm integrity and function, particularly in small ruminants where cryodamage is pronounced. This review explores the molecular mechanisms underlying sperm cryodamage and strategies for improving cryopreservation outcomes, with a focus on the role of antioxidants.
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Cryopreservation poses significant challenges to the preservation of sperm integrity and function, particularly in small ruminants where cryodamage is pronounced. This review explores the molecular mechanisms underlying sperm cryodamage and strategies for improving cryopreservation outcomes, with a focus on the role of antioxidants. Cryopreservation-induced alterations in proteins and RNA transcripts critical for sperm function, including motility, capacitation, fertilization, and embryo development, are discussed. Proteomic, transcriptomic, and epigenomic advancements have provided valuable insights into these mechanisms, offering potential biomarkers for predicting sperm freezability and enhancing cryopreservation strategies. Combining technologies such as mass spectrometry and flow cytometry allows for a comprehensive understanding of molecular and cellular changes induced by the freezing–thawing process. However, challenges remain in optimizing cryoprotectant formulations and antioxidant supplementation to improve post-thaw sperm fertility. Further research is needed to explore a wider range of novel cryoprotectants, antioxidants, and proteins for cryopreservation media, as well as to validate their efficacy in enhancing sperm viability and function. Additionally, investigations into the effects of cryopreservation on RNA transcripts and epigenetic factors in small ruminant species are warranted to advance our understanding of sperm preservation. Overall, this review highlights the importance of antioxidants in mitigating cryodamage and underscores the need for continued research to refine cryopreservation protocols and improve reproductive outcomes in small ruminants.
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Open AccessArticle
Differential Extraction and Preliminary Identification of Polyphenols from Ugni candollei (White Murta) Berries
by
Natalia Fuentes-Jorquera, Roberto I. Canales, José R. Pérez-Correa, Jara Pérez-Jiménez and María Salomé Mariotti-Celis
Antioxidants 2024, 13(6), 623; https://doi.org/10.3390/antiox13060623 - 21 May 2024
Abstract
Ugni candollei, commonly known as white murta, is a native Chilean berry with a polyphenol composition that has been underexplored. This study aimed to establish a comprehensive profile of white murta polyphenols using ultra-performance liquid chromatography electrospray ionization Orbitrap mass spectrometry (UPLC-ESI-ORBITRAP
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Ugni candollei, commonly known as white murta, is a native Chilean berry with a polyphenol composition that has been underexplored. This study aimed to establish a comprehensive profile of white murta polyphenols using ultra-performance liquid chromatography electrospray ionization Orbitrap mass spectrometry (UPLC-ESI-ORBITRAP MS). Additionally, it compared the efficacy of conventional extraction methods with emerging techniques such as deep eutectic solvent (DES) extraction and hot pressurized water extraction (HPWE). The analysis tentatively identified 107 phenolic compounds (84 of them reported for the first time for this cultivar), including 25 phenolic acids, 37 anthocyanins, and 45 flavonoids. Among the prominent and previously unreported polyphenols are ellagic acid acetyl-xyloside, 3-p-coumaroylquinic acid, cyanidin 3-O-(6′-caffeoyl-glucoside, and phloretin 2′-O-xylosyl-glucoside. The study found HPWE to be a promising alternative to traditional extraction of hydroxybenzoic acids, while DES extraction was less effective across all categories. The findings reveal that white murta possesses diverse phenolic compounds, potentially linked to various biological activities.
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(This article belongs to the Section Extraction and Industrial Applications of Antioxidants)
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<p>Sum of areas of the families of phenolic compounds tentatively identified after HPLC-MS analysis in white murta extracts obtained with different extraction procedures. Different letters (a, b, c, and d) represent statistical differences (<span class="html-italic">p</span> < 0.05) between extraction systems for the same polyphenol class. DES: deep eutectic solvent extract; ASE_120: extract with pressurized hot water at 120 °C; ASE_80: extract with pressurized hot water at 80 °C; Conv_1: extract with 50% aqueous methanol; Conv_2: extract with 70% aqueous acetone. HC, hydroxycinnamic acids; HB, hydroxybenzoic acids.</p> Full article ">Figure 2
<p>“White murta hydroxybenzoic acids”. Relative abundance, within the hydroxybenzoic acid family, of the six most abundant phenolic compounds tentatively identified in white murta extracts obtained with different extraction procedures. EAA: ellagic acid arabinoside, EA: ellagic acid, EAAA: ellagic acid acetyl-arabinoside, EAAX: ellagic acid acetyl-xyloside, PCA4OG: protocatechuic acid 4-O-glucoside, GA4OG: gallic acid 4-O-glucoside, GG: galloyl glucose, EAG: ellagic acid glucoside, 5OGQA: 5-O-galloylquinic acid, VAD: valoneic acid dilactone. DES: deep eutectic solvent extract; ASE_120: extract with pressurized hot water at 120 °C; ASE_80: extract with pressurized hot water at 80 °C; Conv_1: extract with 50% aqueous methanol; Conv_2: extract with 70% aqueous acetone.</p> Full article ">Figure 3
<p>“White murta hydroxycinnamic acids”. Relative abundance, within the hydroxycinnamic acid family, of the six most abundant phenolic compounds tentatively identified in white murta extracts obtained with different extraction procedures. CA4OG: p-coumaric acid 4-O-glucoside, pCoG: p-coumaroyl glucose, CA: chlorogenic acid, 3CQA: 3-caffeoylquinic acid, 4CQA: 4-caffeoylquinic acid, 3CoQA: 3-p-coumaroylquinic acid, 4CoQA: 4-p-coumaroylquinic acid, 5CoQA: 5-p-coumaroylquinic acid, FA4OG: ferulic acid 4-O-glucoside, FG: feruloyl glucose, CA4OG: caffeic acid 4-O-glucoside, CG: caffeoyl glucose, pCoTA: p-coumaroyl tartaric acid, 3FQA: 3-feruloylquinic acid, 4FQA: 4-feruloylquinic acid, 5FQA: 5-feruloylquinic acid. DES: deep eutectic solvent extract; ASE_120: extract with pressurized hot water at 120 °C; ASE_80: extract with pressurized hot water at 80 °C; Conv_1: extract with 50% aqueous methanol; Conv_2: extract with 70% aqueous acetone.</p> Full article ">Figure 4
<p>“White murta anthocyanins”. Relative abundance, within the anthocyanin family, of the six most abundant phenolic compounds tentatively identified in white murta extracts obtained with different extraction procedures. Cy3H: cyanidin 3-O-hexoside, Pn3A: peonidin 3-O-arabinoside, Pt3A: petunidin 3-O-arabinoside, Pn3H: peonidin 3-O-hexoside, Mv3A: malvidin 3-O-arabinoside, Dp3P: delphinidin 3-O-pentoside, Cy3O6CG: cyanidin 3-O-(6′-caffeoyl-glucoside), Dp3O6pCoG: delphinidin 3-O-(6′-p-coumaroyl-glucoside), Cy: cyanidin, Pn: peonidin, Pt3H: petunidin 3-O-hexoside. DES: deep eutectic solvent extract; ASE_120: extract with pressurized hot water at 120 °C; ASE_80: extract with pressurized hot water at 80 °C; Conv_1: extract with 50% aqueous methanol; Conv_2: extract with 70% aqueous acetone.</p> Full article ">Figure 5
<p>“White murta flavonoids”. Relative abundance, within the flavonoids family, of the six most abundant phenolic compounds tentatively identified in white murta extracts obtained with different extraction procedures. M3H: myricetin 3-O-hexoside, K3G: kaempferol 3-O-glucuronide, M3R: myricetin 3-O-rhamnoside, Q3H: quercetin 3-O-hexoside, Q4G: quercetin 4′-O-glucoside, M3A: myricetin 3-O-arabinoside, IR3R: isorhamnetin 3-O-rutinoside, IR3G: isorhamnetin 3-O-glucoside, IR7R: isorhamnetin 7-O-rhamnoside, P2XG: phloretin 2′-O-xylosyl-glucoside, K3Gt: kaempferol 3-O-galactoside, Q3R: quercetin 3-O-rhamnoside, 3HP2G: 3-hydroxyphloretin 2′-O-glucoside, DHM3R: dihydromyricetin 3-O-rhamnoside, DHQ3R: dihydroquercetin 3-O-rhamnoside, PhL: phloridzin. DES: deep eutectic solvent extract; ASE_120: extract with pressurized hot water at 120 °C; ASE_80: extract with pressurized hot water at 80 °C; Conv_1: extract with 50% aqueous methanol; Conv_2: extract with 70% aqueous acetone.</p> Full article ">
Full article ">Figure 1
<p>Sum of areas of the families of phenolic compounds tentatively identified after HPLC-MS analysis in white murta extracts obtained with different extraction procedures. Different letters (a, b, c, and d) represent statistical differences (<span class="html-italic">p</span> < 0.05) between extraction systems for the same polyphenol class. DES: deep eutectic solvent extract; ASE_120: extract with pressurized hot water at 120 °C; ASE_80: extract with pressurized hot water at 80 °C; Conv_1: extract with 50% aqueous methanol; Conv_2: extract with 70% aqueous acetone. HC, hydroxycinnamic acids; HB, hydroxybenzoic acids.</p> Full article ">Figure 2
<p>“White murta hydroxybenzoic acids”. Relative abundance, within the hydroxybenzoic acid family, of the six most abundant phenolic compounds tentatively identified in white murta extracts obtained with different extraction procedures. EAA: ellagic acid arabinoside, EA: ellagic acid, EAAA: ellagic acid acetyl-arabinoside, EAAX: ellagic acid acetyl-xyloside, PCA4OG: protocatechuic acid 4-O-glucoside, GA4OG: gallic acid 4-O-glucoside, GG: galloyl glucose, EAG: ellagic acid glucoside, 5OGQA: 5-O-galloylquinic acid, VAD: valoneic acid dilactone. DES: deep eutectic solvent extract; ASE_120: extract with pressurized hot water at 120 °C; ASE_80: extract with pressurized hot water at 80 °C; Conv_1: extract with 50% aqueous methanol; Conv_2: extract with 70% aqueous acetone.</p> Full article ">Figure 3
<p>“White murta hydroxycinnamic acids”. Relative abundance, within the hydroxycinnamic acid family, of the six most abundant phenolic compounds tentatively identified in white murta extracts obtained with different extraction procedures. CA4OG: p-coumaric acid 4-O-glucoside, pCoG: p-coumaroyl glucose, CA: chlorogenic acid, 3CQA: 3-caffeoylquinic acid, 4CQA: 4-caffeoylquinic acid, 3CoQA: 3-p-coumaroylquinic acid, 4CoQA: 4-p-coumaroylquinic acid, 5CoQA: 5-p-coumaroylquinic acid, FA4OG: ferulic acid 4-O-glucoside, FG: feruloyl glucose, CA4OG: caffeic acid 4-O-glucoside, CG: caffeoyl glucose, pCoTA: p-coumaroyl tartaric acid, 3FQA: 3-feruloylquinic acid, 4FQA: 4-feruloylquinic acid, 5FQA: 5-feruloylquinic acid. DES: deep eutectic solvent extract; ASE_120: extract with pressurized hot water at 120 °C; ASE_80: extract with pressurized hot water at 80 °C; Conv_1: extract with 50% aqueous methanol; Conv_2: extract with 70% aqueous acetone.</p> Full article ">Figure 4
<p>“White murta anthocyanins”. Relative abundance, within the anthocyanin family, of the six most abundant phenolic compounds tentatively identified in white murta extracts obtained with different extraction procedures. Cy3H: cyanidin 3-O-hexoside, Pn3A: peonidin 3-O-arabinoside, Pt3A: petunidin 3-O-arabinoside, Pn3H: peonidin 3-O-hexoside, Mv3A: malvidin 3-O-arabinoside, Dp3P: delphinidin 3-O-pentoside, Cy3O6CG: cyanidin 3-O-(6′-caffeoyl-glucoside), Dp3O6pCoG: delphinidin 3-O-(6′-p-coumaroyl-glucoside), Cy: cyanidin, Pn: peonidin, Pt3H: petunidin 3-O-hexoside. DES: deep eutectic solvent extract; ASE_120: extract with pressurized hot water at 120 °C; ASE_80: extract with pressurized hot water at 80 °C; Conv_1: extract with 50% aqueous methanol; Conv_2: extract with 70% aqueous acetone.</p> Full article ">Figure 5
<p>“White murta flavonoids”. Relative abundance, within the flavonoids family, of the six most abundant phenolic compounds tentatively identified in white murta extracts obtained with different extraction procedures. M3H: myricetin 3-O-hexoside, K3G: kaempferol 3-O-glucuronide, M3R: myricetin 3-O-rhamnoside, Q3H: quercetin 3-O-hexoside, Q4G: quercetin 4′-O-glucoside, M3A: myricetin 3-O-arabinoside, IR3R: isorhamnetin 3-O-rutinoside, IR3G: isorhamnetin 3-O-glucoside, IR7R: isorhamnetin 7-O-rhamnoside, P2XG: phloretin 2′-O-xylosyl-glucoside, K3Gt: kaempferol 3-O-galactoside, Q3R: quercetin 3-O-rhamnoside, 3HP2G: 3-hydroxyphloretin 2′-O-glucoside, DHM3R: dihydromyricetin 3-O-rhamnoside, DHQ3R: dihydroquercetin 3-O-rhamnoside, PhL: phloridzin. DES: deep eutectic solvent extract; ASE_120: extract with pressurized hot water at 120 °C; ASE_80: extract with pressurized hot water at 80 °C; Conv_1: extract with 50% aqueous methanol; Conv_2: extract with 70% aqueous acetone.</p> Full article ">
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