[1]周曦,易龙,金鑫,等.SIRT1/UCP2通路在白藜芦醇抑制血管内皮细胞氧化应激损伤中的作用[J].第三军医大学学报,2013,35(16):1671-1675.
 Zhou Xi,Yi Long,Jin Xin,et al.Role of SIRT1/UCP2 signaling pathway in resveratrol-induced inhibition of oxidative injury in vascular endothelial cells[J].J Third Mil Med Univ,2013,35(16):1671-1675.
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SIRT1/UCP2通路在白藜芦醇抑制血管内皮细胞氧化应激损伤中的作用(/HTML )
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《第三军医大学学报》[ISSN:1000-5404/CN:51-1095/R]

卷:
35卷
期数:
2013年第16期
页码:
1671-1675
栏目:
论著
出版日期:
2013-08-30

文章信息/Info

Title:
Role of SIRT1/UCP2 signaling pathway in resveratrol-induced inhibition of oxidative injury in vascular endothelial cells
作者:
周曦易龙金鑫陈明亮陈春烨王丽高燕翔施琳颖糜漫天
第三军医大学军事预防医学院营养与食品安全研究中心,重庆市营养与食品安全重点实验室,重庆市医学营养研究中心
Author(s):
Zhou Xi Yi Long Jin Xin Chen Mingliang Chen Chunye Wang Li Gao Yanxiang Shi Linying Mi Mantian
Center for Nutrition and Food Safety Research, Chongqing Key Laboratory of Nutrition and Food Safety, Chongqing Center of Medical Nutrition Research, College of Military Preventive Medicine, Third Military Medical University, Chongqing, 400038, China
关键词:
动脉粥样硬化白藜芦醇人脐静脉内皮细胞氧化应激SIRT1UCP2
Keywords:
atherosclerosis resveratrol human umbilical vein endothelial cells oxidative stress silent mating type information regulation 2 homolog 1 uncoupling protein 2
分类号:
R151.3;R329.26;R543
文献标志码:
A
摘要:
目的      观察白藜芦醇对血管内皮细胞氧化应激损伤的抑制作用,并围绕SIRT1/UCP2信号通路探讨其作用机制。      方法      原代培养人脐静脉内皮细胞(human umbilical vein endothelial cells,HUVECs),用叔丁基过氧化氢(t-BHP)建立HUVECs氧化应激损伤模型。CCK-8法检测细胞增殖,确定半抑制浓度(IC50)。荧光分光光度计检测细胞内活性氧(ROS)生成。CCK-8法检测白藜芦醇对t-BHP诱导的HUVECs活力的影响;qRT-PCR法检测白藜芦醇对SIRT1和UCP2 mRNA表达的影响;Western blot法检测白藜芦醇对SIRT1、UCP2和Caspase-3在细胞内蛋白表达的影响。      结果      t-BHP明显抑制细胞活力,IC50为80 μmol/L。白藜芦醇(0.1、1、10 μmol/L)预处理2 h能显著抑制t-BHP诱导的细胞活力下降(P<0.05),并抑制t-BHP诱导的细胞内ROS增加(P<0.05)。同时,白藜芦醇能明显抑制t-BHP诱导的SIRT1的mRNA和蛋白表达下降、UCP2的mRNA和蛋白表达升高及Caspase-3表达增加(P<0.05),而Sirt1抑制剂尼克酰胺能削弱白藜芦醇的抑制作用。      结论      白藜芦醇可能通过活化SIRT1抑制UCP2表达,削弱t-BHP诱导的细胞内ROS生成,从而抑制血管内皮细胞氧化应激损伤。
Abstract:
Objective      To assess the role of silent mating type information regulation 2 homolog 1/uncoupling protein 2 (SIRT1/UCP2) signaling pathway in the inhibition of oxidative damage in vascular endothelial cells by resveratrol.        Methods      Human umbilical vein endothelial cells (HUVECs) were isolated and primarily cultured. The obtained cells were treated by tert-butyl hydroperoxide (t-BHP) at the concentrations of 20, 30, 40, 50, 60, 70, 80, 90 and 100 μmol/L respectively for 24 h, and CCK-8 assay was used for cell viability to determine the IC50 value. The intracellular level of reactive oxygen species (ROS) was observed by fluorospectrophotometry. The expression of SIRT1 and UCP2 at mRNA level was determined by qRT-PCR assay. The protein expression of SIRT1, UCP2 and Caspase-3 were determined by Western blot assay.       Results      Cell viability was significantly inhibited by t-BHP treatment (P<0.05)and the IC50 value was identified as 80 μmol/L. Pretreatment with resveratrol at the doses of 0.1, 1, and 10 μmol/L significantly inhibited the decrease of cell viability (P<0.05) and the increase of intracellular ROS level induced by t-BHP. Furthermore, the mRNA and protein expression of SIRT1 were up-regulated by resveratrol pretreatment, and that of UCP2 was down-regulated, yet which was abolished by niacinamide pretreatment.       Conclusion      Resveratrol may suppress the expression of UCP2 by activating SIRT1, and attenuate the increase of intracellular ROS level induced by t-BHP, and thus, inhibit t-BHP-induced endothelial injury.

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更新日期/Last Update: 2013-08-02