| 注册
首页|期刊导航|重庆医学|PI3K/Akt-NO信号通路在Ang Ⅳ诱导大鼠心肌肥大中的作用

PI3K/Akt-NO信号通路在Ang Ⅳ诱导大鼠心肌肥大中的作用

彭晓凤 陈加飞 王全华 周龙洋 王佳 蒋青松

重庆医学2012,Vol.41Issue(11):1055-1057,1061,4.
重庆医学2012,Vol.41Issue(11):1055-1057,1061,4.DOI:10.3969/j.issn.1671-8348.2012.11.005

PI3K/Akt-NO信号通路在Ang Ⅳ诱导大鼠心肌肥大中的作用

Effect of PI3K/Akt-NO signal pathway on cardiomyocyte hypertrophy induced by angiotensin IV in rats

彭晓凤 1陈加飞 2王全华 3周龙洋 1王佳 1蒋青松1

作者信息

  • 1. 重庆医科大学药理学教研室,400016
  • 2. 重庆市巴南区人民医院药剂科,401320
  • 3. 重庆市綦江县人民医院药剂科,401420
  • 折叠

摘要

Abstract

Objective To study the effect of PI3/Akt-NO signal transduction pathway on cardiomyocyte hypertrophy induced by angiotensin IV (Ang IV ) .Methods The cardiomyocyte hypertrophy responses were assayed by measuring the cell surface area and atrial natriuretic factor mRNA expression in cultured neonatal rat cardiomyocytes .NO concentration and endothelial NO syn-thase (eNOS) activity were determined by using the nitrate reduction and ELISA methods ,respectively .The mRNA and protein expressions were detected by real-time PCR and western blotting respectively .In cultured cardiomyocytes ,LY294002 ,a selective PI3K antagonist ,and L-NAME ,a selective NOS antagonist ,were used to investigate the mechanisms of Ang IV .Results In cultured cardiomyocytes,Ang Ⅳ (0 .01,0 .1 ,1 nmol/L) induced cardiomyocyte hypertrophy in a concentration-dependent way .Meanwhile ,the expressions of Akt mRNA and protein decreased ,and the expression of eNOS mRNA and the concentrations of eNOS and NO reduced (P<0 .05) .LY294002 and L-NAME enhanced these effects of Ang Ⅳ (P<0 .05) .Conclusion PIsK/Akt-NO signal transduction pathway involves in cardiomyocyte hypertrophy induced by Ang Ⅳ,at least partly .

关键词

血管紧张素Ⅳ/PI3K/Akt信号通路/心肌肥大

Key words

angiotensin Ⅳ/ PI3 K/Akt/ signal pathway/ cardiomyoeyte hypertrophy

引用本文复制引用

彭晓凤,陈加飞,王全华,周龙洋,王佳,蒋青松..PI3K/Akt-NO信号通路在Ang Ⅳ诱导大鼠心肌肥大中的作用[J].重庆医学,2012,41(11):1055-1057,1061,4.

基金项目

国家自然科学基金资助项目(NSFC,81100905) (NSFC,81100905)

高等学校博士学科点专项科研基金资助项目(20105503120005). (20105503120005)

重庆医学

OA北大核心CSCDCSTPCD

1671-8348

访问量0
|
下载量0
段落导航相关论文