缬沙坦对超负荷大鼠心肌细胞凋亡、ASK1的影响

邱敏; 马康华; 龙明智; 谭晓; 王迪斌

doi:10.13406/j.cnki.cyxb.2007.05.013

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缬沙坦对超负荷大鼠心肌细胞凋亡、ASK1的影响

论著 | 更新时间：2024-01-17

- 缬沙坦对超负荷大鼠心肌细胞凋亡、ASK1的影响
- Effects of Valsartan on cardiomyocyte apoptosis and ASK1 protein expression in pressure overload-induced cardiac hypertrophy in rats
- 重庆医科大学学报 2007年第5期页码：493-496
- 作者机构：
  
  1. 南京医科大学第二附属医院心内科
  2. 重庆医科大学附属第一医院心内科
- 作者简介：
- 基金信息：
- DOI：10.13406/j.cnki.cyxb.2007.05.013
  中图分类号： R541.3
- 纸质出版日期：2007，
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[1]邱敏,马康华,龙明智,谭晓,王迪斌.缬沙坦对超负荷大鼠心肌细胞凋亡、ASK1的影响[J].重庆医科大学学报,2007(05):493-496+510.

Effects of Valsartan on cardiomyocyte apoptosis and ASK1 protein expression in pressure overload-induced cardiac hypertrophy in rats[J]. Journal of Chongqing Medical University, 2007,(5):493-496.
[1]邱敏,马康华,龙明智,谭晓,王迪斌.缬沙坦对超负荷大鼠心肌细胞凋亡、ASK1的影响[J].重庆医科大学学报,2007(05):493-496+510. DOI： 10.13406/j.cnki.cyxb.2007.05.013.

Effects of Valsartan on cardiomyocyte apoptosis and ASK1 protein expression in pressure overload-induced cardiac hypertrophy in rats[J]. Journal of Chongqing Medical University, 2007,(5):493-496. DOI： 10.13406/j.cnki.cyxb.2007.05.013.

摘要

目的:探讨压力超负荷模型下血管紧张素Ⅱ（AngⅡ）受体拮抗剂缬沙坦对凋亡信号调节激酶（ASKl）介导心肌肥厚信号通路的影响。方法:复制腹主动脉缩窄高血压大鼠模型

TUNEL法检测心肌细胞凋亡

免疫印迹和免疫组化法检测心肌ASKl蛋白含量并测定左室质量指数。结果:缬沙坦组左心室质量指数、心肌细胞凋亡指数、ASKl表达均显著低于高血压组（P<0.05）。结论:AngⅡ参与激活压力负荷下ASKl通路

缬沙坦能干预ASKl介导通路并抑制心肌细胞凋亡从而预防心肌肥厚。

Abstract

Objective:To determine the effects of Valsartan on cardiomyocyte apoptosis and apoptosis signal-regulating kinase 1 (ASK1)-dependent signal pathway in cardiac pressure-overload hypertrophy.Methods:The hypertensive model was established by abdominal aortic constriction.24 wistar rats were randomized into three groups

banding group

banding and Valsartan admin- istration group

sham-operated group.Six weeks later

cardiomyocyte apoptosis was measured by TUNEL

ASKI protein expres- sion was measured by western blot and immunohistochemistry.Results:The left ventricular mass index

apoptosis index and ASKI protein content all significantly decreased in Valsartan group

as compared with banding group(P<0.05).Conclusion: AngⅡis involved in promoting the activation of ASK1-dependent signal pathway in pressure-overload model.

关键词

心肌肥厚凋亡信号调节激酶凋亡管紧张素Ⅱ缬沙坦

Keywords

myocardial hypertrophyASK1apoptosisAngllvalsartan

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