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Resveratrol reduces intracellular reactive oxygen species levels by inducing autophagy through the AMPK-mTOR pathway
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نویسنده
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Jun Song ,Yeping Huang ,Wenjian Zheng ,Jing Yan ,Min Cheng ,Ruxing Zhao ,Li Chen ,Cheng Hu ,Weiping Jia
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منبع
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frontiers of medicine - 2018 - دوره : 12 - شماره : 6 - صفحه:697 -706
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چکیده
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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.
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کلیدواژه
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resveratrol ,reactive oxygen species ,AMPK ,mTOR ,autophagy
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آدرس
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Qilu Hospital of Shandong University, Department of Endocrinology, China. Tongji University School of Medicine, Department of Endocrinology, China. Shanghai Jiao Tong University Affiliated Sixth People’s Hospital, Shanghai Key Laboratory of Diabetes Mellitus, China, Shanghai Jiao Tong University Affiliated Sixth People’s Hospital, Shanghai Key Laboratory of Diabetes Mellitus, China, city:Qingdao, Department of Geriatrics, Qingdao Haici Medical Treatment Group, China, Shanghai Jiao Tong University Affiliated Sixth People’s Hospital, Shanghai Key Laboratory of Diabetes Mellitus, China, Huangdao Disease Prevention and Control Center, China, Qilu Hospital of Shandong University, Department of Endocrinology, China, Qilu Hospital of Shandong University, Department of Endocrinology, China, Shanghai Jiao Tong University Affiliated Sixth People’s Hospital, Shanghai Key Laboratory of Diabetes Mellitus, China, Shanghai Jiao Tong University Affiliated Sixth People’s Hospital, Shanghai Key Laboratory of Diabetes Mellitus, China
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Authors
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