The Mechanism Of Resveratrol Provents H9c2Cells From Oxidative Stress That Induced By H2O2and Its Relationship With Autophagy

Recently, many studies have attempted to illustrate the mechanism of autophagy in protection against oxidative stress to the heart induced by H₂O₂. However, whether resveratrol-induced autophagy involves the p38-MAPK pathway is still unknown. This study aimed to investigate whether treating H9c2cells with resveratrol increases autophagy and attenuates the cell death and apoptosis induced by oxidative stress via the p38-MAPK pathway. Resveratrol with or without SB202190, an inhibitor of the p38MAPK pathway, was added30min before H₂O₂. After H₂O₂treatment, the cells were incubated under5%CO₂at37℃for24h to assess cell survival and death, or incubated for20min for Western blot and transmission electron microscopy. Flow cytometry was used to detect apoptosis after6h of H₂O₂treatment. Resveratrol at20μmol/L protected H9c2cells treated with100μmol/L H₂O₂from oxidative damage. It increased cell survival and markedly decrease lactate dehydrogenase release. In addition, resveratrol increased autophagy and decreased H₂O₂-induced apoptosis. Furthermore, the protective effects of resveratrol were inhibited by10μmol/L SB202190. Thus, resveratrol protected H₂O₂-treated H9c2cells by up-regulating autophagy via the p38-MAPK pathway.