卡托普利和氯沙坦对血管紧张素Ⅱ诱导血管平滑肌细胞Bcl2和Fas基因表达的抑制作用  

Inhibitory effects of Captopril and Losartan on expression of Bcl-2 and Fas induced by AngⅡ

作　　者：李劲迈[1] 朱清[1] 岳欣[1] 贺红[1] 

机构地区：[1]山东大学齐鲁医院心内科,济南250012

出　　处：《山东大学学报（医学版）》2009年第12期25-28,共4页Journal of Shandong University:Health Sciences

基　　金：山东省科技攻关计划资助项目(22130163)

摘　　要：目的研究卡托普利(CP)和氯沙坦(LT)及血管紧张素Ⅱ(AngⅡ)对Wistar大鼠血管平滑肌细胞(VSMC)凋亡相关基因表达的影响。方法采用流式细胞技术检测CP、LT及CP与LT联合应用对在AngⅡ不同浓度、不同作用时间下体外培养的大鼠主动脉VSMC凋亡相关基因Bcl-2及Fas的表达量。结果随着AngⅡ作用浓度的增加和作用时间的延长,Bcl-2基因表达量增加且呈浓度和作用时间依赖(P<0.01);AngⅡ可使Fas的表达量增加(P<0.05),但无明显时间和浓度依赖性;一定浓度的CP(5×10-6mol/L)和LT(5×10-6mol/L)可抑制AngⅡ对2个基因表达的影响。(P均<0.05或P均<0.01)。结论CP和LT可以通过拮抗VSMC凋亡基因Bcl-2和Fas的表达促进异常增殖的VSMC凋亡,且这一作用与作用浓度和作用时间相关。Objective To investigate expression of genes associated with the apoptosis of Wistar rat vascular smooth muscle cell（VSMC）affected by AngⅡ,Captopril（CP）,and Losartan（LT）.Methods Expressions of genes associated with appotosis induced by AngⅡwith different concentrations and action times in in vitro rat aorta VSMC were detected by flow cytometry.Results Expression of Bcl-2 was up-regulated by AngⅡ in a dose-and time-related manner（P〈0.01）.Expression of Fas.was down-regulated（P〈0.05）,but not in an apparent time-and dose-related manner.CP and LT inhibited the action of AngⅡ（P〈0.05 or P〈0.01）.Conclusion CP（5×10^-6mol/L）and LT（5×10^-6mol/L）can withstand expressions of Bcl-2 and Fas induced by AngⅡ and promote the apoptosis of abnormal hyperplastic VSMCs,which is partly related to the concentration and reaction time.

关 键 词：细胞凋亡 血管紧张素Ⅱ 基因 肌 平滑 血管 

分 类 号：Q95-33[生物学—动物学]