ArticleEuropean journal of nutrition2014
Eicosapentaenoic acid attenuated oxidative stress-induced cardiomyoblast apoptosis by activating adaptive autophagy.
Article in European journal of nutrition, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 26 citations in OpenAlex.
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- Quantitative Profiling of Oxylipin Reveals the Mechanism of Pien-Tze-Huang on Alcoholic Liver Disease.Evidence-based complementary and alternative medicine : eCAM · 2021Article
- Signaling and other functions of lipids in autophagy: a review.Lipids in health and disease · 2020Review
- High-Dose Paraquat Induces Human Bronchial 16HBE Cell Death and Aggravates Acute Lung Intoxication in Mice by Regulating Keap1/p65/Nrf2 Signal Pathway.Inflammation · 2019Article
- Alpha linolenic acid decreases apoptosis and oxidized phospholipids in cardiomyocytes during ischemia/reperfusion.Molecular and cellular biochemistry · 2018Article
- Protective Effects of ω-3 PUFA in Anthracycline-Induced Cardiotoxicity: A Critical Review.International journal of molecular sciences · 2017Review
- High-fat diet induces cardiomyocyte apoptosis via the inhibition of autophagy.European journal of nutrition · 2016Article
- Eicosapentaenoic acid attenuates dexamethasome-induced apoptosis by inducing adaptive autophagy via GPR120 in murine bone marrow-derived mesenchymal stem cells.Cell death & disease · 2016Article
- Article
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeRecently, several large, randomized clinical trials have proven the benefits of eicosapentaenoic acid (EPA) in cardiovascular prevention. However, the precise protective mechanisms of EPA for heart disease are still controversial. In this study, we evaluate the possible protective effects of EPA, especially the role of autophagy, against cardiomyocyte apoptosis induced by oxidative stress.
methodsH9C2 myocardioblasts were incubated with 80 μM EPA for 24 h and then exposed to 400 μM of hydrogen peroxide for 3 h. Autophagic response, lysosome function, and apoptosis were analyzed at the end of the experiment.
resultsPreincubation of EPA significantly inhibited apoptosis and increased cell viability for H9C2 cells under oxidative stress. The effects of EPA on apoptosis and cell viability were suppressed by 3-MA treatment (autophagic inhibitor). Oxidative stress decreased Beclin 1 protein expression, increased the ratio of LC3II/LC3I, and reduced the formation of acid organelles, whereas the preincubation of EPA abrogated the negative effect of oxidative stress on H9C2 by mediating the autophagic response. Inhibiting autophagy by 3-methyladenine reversed the EPA effect significantly by increasing the ratio of LC3II-LC3I. Treatment with 3-MA did not alter the increment of acid organelles by EPA preincubation. In addition, EPA restored the phosphorylation of Akt activated by H2O2 treatment and induced the phosphorylation of AMPK in H9C2 cells under oxidative stress.
conclusionEPA attenuated oxidative stress-induced cardiomyocyte apoptosis by activating an adaptive autophagic response.
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