Resveratrol reduces intracellular reactive oxygen species levels by inducing autophagy through the AMPK-mTOR pathway

Abstract

Oxidative stress induced by free fatty acid aggravates endothelial injury, which leads to diabetic cardiovascular complications. Reduction of intracellular oxidative stress may attenuate these pathogenic processes. The dietary polyphenol resveratrol reportedly exerts potential protective effects against endothelial injury. This study determined whether resveratrol can reduce the palmitic acid (PA)-induced generation of reactive oxygen species (ROS) and further explored the underlying molecular mechanisms. We found that resveratrol significantly reduced the PA-induced endothelial ROS levels in human aortic endothelial cells. Resveratrol also induced endothelial cell autophagy, which mediated the effect of resveratrol on ROS reduction. Resveratrol stimulated autophagy via the AMP-activated protein kinase (AMPK)-mTOR pathway. Taken together, these data suggest that resveratrol prevents PA-induced intracellular ROS by autophagy regulation via the AMPK-mTOR pathway. Thus, the induction of autophagy by resveratrol may provide a novel therapeutic candidate for cardioprotection in metabolic syndrome.

Keywords

resveratrol / reactive oxygen species / AMPK / mTOR / autophagy

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Acknowledgements

The present work was funded by outstanding young scientist research grant in Shandong Province (No. 2013BSE27128), National Natural Science Foundation of China (No. 81370943), China Postdoctoral Science Foundation (No. 2015M580334) and Shanghai Municipal Health and Family Planning Commission Project (No. 20134189).

Compliance with ethics guidelines

Jun Song, Yeping Huang, Wenjian Zheng, Jing Yan, Ming Cheng, Ruxing Zhao, Li Chen, Cheng Hu, and Weiping Jia declare no conflict of interest. We followed all institutional and national guidelines for the care and use of laboratory animal.

Electronic Supplementary Material

Supplementary material is available in the online version of this article at https://doi.org/ 10.1007/s11684-018-0655-7 and is accessible for authorized users.

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