title: Resveratrol reduces vascular cell senescence through attenuation of oxidative stress by SIRT1/NADPH oxidase-dependent mechanisms.
abstract: OBJECTIVE
  Senescence of vascular cells contributes to the development of cardiovascular diseases and the overall aging. This study was undertaken to investigate the effects of resveratrol (Res) on amelioration of vascular cell aging and the role of SIRT1/nicotinamide adenine dinucleotide phosphate (NADPH) oxidase pathway.
  
  
  RESULTS
  Adult male Wistar rats were treated with a high-fat/sucrose diet (HFS) in the presence or absence of Res for 3 months. HFS and in vitro treatment with high glucose increased the senescence cells and reactive oxygen species production in rat aorta and cultured bovine aortic endothelial cells (BAECs), respectively, which was attenuated by Res treatment. Res protected against HFS- or high-glucose-induced increase in NADPH oxidase p47phox expression and decrease in SIRT1 level. Apocynin, a NADPH oxidase inhibitor, down-regulated p47phox protein expression, but had no influence on SIRT1 protein; sirtinol, a SIRT1 inhibitor, aggravated the decrease in SIRT1 protein level and the increase in p47phox protein expression induced by high glucose.
  
  
  CONCLUSIONS
  Our studies suggested that Res was able to reverse the senescence process in aorta induced by HFS in rats or induced by the exposure to high glucose in cultured BAECs. The underlying mechanism is at least SIRT1/NADPH oxidase pathway dependent.
authors.affiliation: Department of Nutrition and Food Hygiene, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, Hubei, PR China.
authors.forename: Yuhan
authors.initials: Y
authors.lastname: Tang
authors.forename: Jian
authors.initials: J
authors.lastname: Xu
authors.forename: Wei
authors.initials: W
authors.lastname: Qu
authors.forename: Xiaolin
authors.initials: X
authors.lastname: Peng
authors.forename: Peng
authors.initials: P
authors.lastname: Xin
authors.forename: Xuefeng
authors.initials: X
authors.lastname: Yang
authors.forename: Chenjiang
authors.initials: C
authors.lastname: Ying
authors.forename: Xiufa
authors.initials: X
authors.lastname: Sun
authors.forename: Liping
authors.initials: L
authors.lastname: Hao
mesh_terms: D000818:Animals; D001011:Aorta / Q000166:cytology / Q000187:drug effects; D001835:Body Weight / Q000187:drug effects; D002417:Cattle; D002478:Cells, Cultured; D016922:Cellular Senescence / Q000187:drug effects*; D059305:Diet, High-Fat / Q000009:adverse effects; D004730:Endothelium, Vascular / Q000166:cytology* / Q000187:drug effects; D005947:Glucose / Q000009:adverse effects; D008055:Lipids / Q000097:blood; D008297:Male; D019255:NADPH Oxidases / Q000378:metabolism*; D018384:Oxidative Stress / Q000187:drug effects*; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000378:metabolism; D000077185:Resveratrol; D056564:Sirtuin 1 / Q000378:metabolism*; D013267:Stilbenes / Q000494:pharmacology*
chemical_list: D008055:Lipids; D017382:Reactive Oxygen Species; D013267:Stilbenes; D019255:NADPH Oxidases; C060505:neutrophil cytosolic factor 1; C488368:Sirt1 protein, rat; D056564:Sirtuin 1; D005947:Glucose; D000077185:Resveratrol