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阿托伐他汀对同型半胱氨酸诱导内皮细胞内质网应激的抑制作用
引用本文:贾方,孙建辉,吴春芳,陈桢玥,陆国平.阿托伐他汀对同型半胱氨酸诱导内皮细胞内质网应激的抑制作用[J].江苏大学学报(医学版),2012,22(6):483-486,490.
作者姓名:贾方  孙建辉  吴春芳  陈桢玥  陆国平
作者单位:(1.常州市第一人民医院心内科, 江苏常州 213003; 2.上海交通大学医学院附属瑞金医院心脏科, 上海 200025)
摘    要:目的: 观察阿托伐他汀对同型半胱氨酸(Hcy)诱导的人脐静脉内皮细胞内质网应激(endoplasmic reticulum stress,ERS)以及凋亡的影响。方法: 不同浓度的Hcy或联合阿托伐他汀处理人脐静脉内皮细胞后,流式细胞术检测细胞凋亡率,实时定量PCR和蛋白质印迹法测定ERS相关分子BiP、CHOP及p-eIF2α、p- PERK的表达变化。结果: Hcy呈浓度依赖性地诱导内皮细胞ERS相关分子BiP、CHOP及p-eIF2α、p-PERK的表达,阿托伐他汀可明显抑制Hcy诱导的内皮细胞ERS相关分子的表达,减少内皮细胞凋亡。结论: 阿托伐他汀可通过下调ERS相关信号通路,抑制Hcy诱导的人脐静脉内皮细胞凋亡。

关 键 词:阿托伐他汀  同型半胱氨酸    内质网应激    动脉粥样硬化  人脐静脉内皮细胞  
收稿时间:2012-07-23

Inhibitive effects of atorvastatin on homocysteine-induced endoplasmicreticulum stress in human umbilical vein endothelial cells
JIA Fang , SUN Jian-hui , WU Chun-fang , CHEN Zhen-yue , LU Guo-ping.Inhibitive effects of atorvastatin on homocysteine-induced endoplasmicreticulum stress in human umbilical vein endothelial cells[J].Journal of Jiangsu University Medicine Edition,2012,22(6):483-486,490.
Authors:JIA Fang  SUN Jian-hui  WU Chun-fang  CHEN Zhen-yue  LU Guo-ping
Institution:(1.Department of Cardiology,the First People′s Hospital of Changzhou, Changzhou Jiangsu 213003; 2.Department of Cardiology, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200025)
Abstract:Objective: To examine the effects of atorvastatin on homocysteine(Hcy)-induced endoplasmic reticulum stress (ERS) activation and cell apoptosis in human umbilical vein endothelial cells (HUVECs). Methods: HUVECs were incubated with various concentrations of Hcy in the presence or absence of atorvastatin. Apoptosis rate was recorded, and expression levels of ERS markers(BiP, CHOP, p-eIF2α and p PERK) were measured by real-time PCR and Western blot analysis. Results Hcy increased the expression of ERS markers in a dose-dependent manner. Atorvastatin could suppress ERS activation and decrease the apoptosis induced by Hcy in HUVECs. Conclusion: Atorvastatin inhibited Hcy-induced ERS in HUVECs. The protective effect of atorvastatin against Hcy induced apoptosis was partially mediated by ERS inhibition.
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