Why the study?
Does resveratrol prevent doxorubicin-induced apoptosis in H9c2 cells?
Does resveratrol prevent doxorubicin-induced apoptosis in H9c2 cells?
Resveratrol protects cardiomyocytes from doxorubicin-induced apoptosis by activating the AMPK/P53 pathway.
May protect cardiomyocytes from doxorubicin via AMPK/P53; leaves open clinical translation from cell models.
Doxorubicin (DOX) is an efficient drug used in cancer therapy; however, it has severe cardiotoxic side effects. The aim of the present study was to investigate the effects of resveratrol on the adenosine monophosphate-activated protein kinase (AMPK)/P53 pathway in mediating DOX-induced cytotoxicity. H9c2 cells were exposed to 5 µM DOX for 24 h to establish a model of DOX-induced cardiotoxicity. DOX administration amplified P53 and B-cell lymphoma 2 (Bcl-2)-associated X protein (Bax) expression and decreased Bcl-2 expression in H9c2 cells. Resveratrol increased the cell viability and decreased the apoptotic rate. In addition, resveratrol markedly increased the phosphorylation of AMPK. Of note, resveratrol protected against DOX-induced increases of P53 and Bax and also prevented the downregulation of Bcl-2 in H9c2 cells. Furthermore, AMPK inhibitor Compound C abolished the protective effects of resveratrol. The results of the present study therefore indicated that resveratrol protected H9c2 cells from DOX-induced apoptosis via the AMPK/P53 pathway.
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Liu et al. (2015) studied this question.
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