Resveratrol reduces intracellular reactive oxygen species levels by inducing autophagy through the AMPK-mTOR pathway.
10.1007/s11684-018-0655-7
- Author:
Jun SONG
1
;
Yeping HUANG
1
;
Wenjian ZHENG
2
;
Jing YAN
1
;
Min CHENG
3
;
Ruxing ZHAO
4
;
Li CHEN
4
;
Cheng HU
5
;
Weiping JIA
6
Author Information
1. Shanghai Diabetes Institute, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Key Clinical Center for Metabolic Diseases, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, 200233, China.
2. Department of Geriatrics, Qingdao Haici Medical Treatment Group, Qingdao, 266000, China.
3. Huangdao Disease Prevention and Control Center, Qingdao, 266555, China.
4. Department of Endocrinology, Qilu Hospital of Shandong University, Jinan, 250012, China.
5. Shanghai Diabetes Institute, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Key Clinical Center for Metabolic Diseases, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, 200233, China. alfredhc@sjtu.edu.cn.
6. Shanghai Diabetes Institute, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Key Clinical Center for Metabolic Diseases, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, 200233, China. wpjia@sjtu.edu.cn.
- Publication Type:Journal Article
- Keywords:
AMPK;
autophagy;
mTOR;
reactive oxygen species;
resveratrol
- MeSH:
AMP-Activated Protein Kinases;
metabolism;
Animals;
Antioxidants;
pharmacology;
Autophagy;
drug effects;
Cells, Cultured;
Endothelial Cells;
Humans;
Male;
Mice;
Mice, Inbred C57BL;
Oxidative Stress;
drug effects;
Reactive Oxygen Species;
metabolism;
Resveratrol;
pharmacology;
Signal Transduction;
drug effects;
TOR Serine-Threonine Kinases;
metabolism
- From:
Frontiers of Medicine
2018;12(6):697-706
- CountryChina
- Language:English
-
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.
