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白藜芦醇通过 SIRT1/NADPH 氧化酶依赖性机制减轻氧化应激,从而减少血管细胞衰老。

Resveratrol reduces vascular cell senescence through attenuation of oxidative stress by SIRT1/NADPH oxidase-dependent mechanisms.

机构信息

Department of Nutrition and Food Hygiene, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, Hubei, PR China.

出版信息

J Nutr Biochem. 2012 Nov;23(11):1410-6. doi: 10.1016/j.jnutbio.2011.08.008. Epub 2012 Jan 27.

DOI:10.1016/j.jnutbio.2011.08.008
PMID:22284404
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.

METHODS AND 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.

CONCLUSION

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.

摘要

目的

血管细胞衰老会导致心血管疾病和整体衰老的发生。本研究旨在探讨白藜芦醇(Res)对改善血管细胞衰老的作用及其与 SIRT1/烟酰胺腺嘌呤二核苷酸磷酸(NADPH)氧化酶途径的关系。

方法和结果

雄性 Wistar 大鼠给予高脂肪/蔗糖饮食(HFS)并同时或不同时给予白藜芦醇处理 3 个月。HFS 和高糖体外处理分别增加了大鼠主动脉和牛主动脉内皮细胞(BAECs)中的衰老细胞和活性氧的产生,而白藜芦醇处理则减轻了这种作用。白藜芦醇可防止 HFS 或高葡萄糖引起的 NADPH 氧化酶 p47phox 表达增加和 SIRT1 水平降低。NADPH 氧化酶抑制剂 apocynin 下调了 p47phox 蛋白表达,但对 SIRT1 蛋白没有影响;SIRT1 抑制剂 sirtinol 加重了高葡萄糖诱导的 SIRT1 蛋白水平降低和 p47phox 蛋白表达增加。

结论

本研究表明,白藜芦醇能够逆转 HFS 诱导的大鼠主动脉或高葡萄糖诱导的培养 BAECs 衰老过程。其潜在机制至少部分依赖于 SIRT1/NADPH 氧化酶途径。

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