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Biochem Biophys Res Commun. 2013 Aug 23;438(2):270-6. doi: 10.1016/j.bbrc.2013.07.042. Epub 2013 Jul 24.

Resveratrol protects cardiomyocytes from oxidative stress through SIRT1 and mitochondrial biogenesis signaling pathways.

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  • 1Division of Cardiology, Shanghai Sixth Hospital, Shanghai Jiao Tong University, School of Medicine, State Key Discipline Division, 600 Yishan Rd., Shanghai 200233, People's Republic of China. liyongguang222326@163.com

Abstract

Reactive oxygen species (ROS) is generated by oxidative stress and plays an important role in various cardiac pathologies. The SIRT1 signaling pathway and mitochondrial biogenesis play essential roles in mediating the production of ROS. SIRT1 activated by resveratrol protects cardiomyocytes from oxidative stress, but the exact mechanisms by which SIRT1 prevents oxidative stress, and its relationship with mitochondrial biogenesis, remain unclear. In this study, it was observed that after stimulation with 50μMH2O2 for 6h, H9C2 cells produced excessive ROS and downregulated SIRT1. The mitochondrial protein NDUFA13 was also downregulated by ROS mediated by SIRT1. Resveratrol induced the expression of SIRT1 and mitochondrial genes NDUFA1, NDUFA2, NDUFA13 and Mn-SOD. However, the production of these genes was reversed by SIRT1 inhibitor nicotinamide. These results suggest that resveratrol inhibits ROS generation in cardiomyocytes via SIRT1 and mitochondrial biogenesis signaling pathways.

Copyright © 2013 Elsevier Inc. All rights reserved.

KEYWORDS:

3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide; Cardiomyocytes; DCF; DMEM; DMSO; Dulbecco’s Modified Eagle Medium; FBS; MTT; Mitochondria; NAM; ROS; Reactive oxygen species; Resveratrol; SIRT1; dimethyl sulfoxide; fetal bovine serum; fluorescent dichlorofluorescein; nicotinamide; reactive oxygen species

[PubMed - indexed for MEDLINE]
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