Abstract
Recently, 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. H9C2 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. Preincubation 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. EPA attenuated oxidative stress-induced cardiomyocyte apoptosis by activating an adaptive autophagic response.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.