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|本期目录/Table of Contents|

IPC和缬沙坦在心肌缺血/再灌注损伤中的作用

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2009年第1期
页码:
11
栏目:
基础研究
出版日期:
2009-02-28

文章信息/Info

Title:
Role of IPC and valsartan in myocardial ischemia reperfusion injury
作者:
寇俊杰; 王爱华; 卫丹; 洪小剑; 武英彪
哈尔滨医科大学第一临床医学院心内四科,黑龙江 哈尔滨 150001
Author(s):
KOU Jun-jie;  WANG Ai-hua;  WEI Dan;  HONG Xiao-jian;  WU Ying-biao
Fourth Department of Cardiology, First Clinical Hospital, Haerbin Medical University, Haerbin 150001, Heilongjiang, China
关键词:
缺血/再灌注损伤; 缺血预适应; 缬沙坦; 信号转导及转录激活因子3
Keywords:
ischemia-reperfusion;  ischemic precondition;  valsartan;  signal transducer and activator of transcription 3
分类号:
R542.4
DOI:
-
文献标识码:
A
摘要:
目的 研究缺血预适应（ischemic preconditioning，IPC）和缬沙坦(valsartan)在缺血/再灌注(I/R)损伤时与信号转导及转录激活因子3(STAT3)的关系，及其对心脏的保护作用。方法 将32只Wistar 大鼠随机分为4组(每组8只),分别为I/R组、IPC组、缬沙坦I/R（VIR）组、和缬沙坦IPC（VIPC）组，I/R组和IPC组合称为生理盐水组，VIR组和VIPC组合称为缬沙坦组。用ELISA方法检测血清IL-6的水平,并留取梗死区心肌组织用免疫组化染色法，检测STAT3 的磷酸化。结果 IPC 组与I/R组相比，STAT3的磷酸化明显增加(P<0.01)，IL-6 的水平降低(P<0.01)。缬沙坦组与生理盐水组相比，STAT3的磷酸化和血清IL-6的水平明显降低(P<0.01)。结论 IPC通过STAT3磷酸化，可激活心肌存活通路，抑制炎症因子的表达，减轻I/R损伤。缬沙坦可部分抑制STAT3 活化，抑制IL-6的表达，并产生心脏保护作用。
Abstract:
AIM To study the relationship between ischemia precondition (IPC)/valsartan and signal transducer and activator of transcription 3 (STAT3) in ischemia-reperfusion (I/R) injury and to explore their role in myocardial protection. METHODS Thirty-two healthy male Wistar rats were randomly divided into four groups (I/R, IPC, VIR and VIPC groups). I/R and IPC were induced by intragastric administration with isotonic Na chloride for 1 week, and then I/R was subjected to 30 min of sustained ischemia by occluding the left anterior descending coronary artery (LAD) and 1 hour of reperfusion. IPC underwent 3 cycles of 5-minute occlusion and reperfusion of LAD before the experiment continued as I/R. VIR and VIPC were induced by intragastric administration with valsartan for 1 week (30 mg/kg), and then VIR continued as I/R, and VIPC continued as IPC. The pectoral cavity was opened to take blood from the right cardiac ventricle. Blood was centrifugated and serum was obtained to detect IL-6 by ELISA. Myocardial tissues in infarcted domain were obtained to detect phosphorylation of STAT3 by immunohistochemistry. RESULTS The phosphorylation of STAT3 was increased and the expression of IL-6 was degraded in IPC group compared to those in I/R group (P<0.01). The phosphorylation of STAT3 and the expression of IL-6 both were downregulated in Valsartan group compared to those in normal saline group (P<0.01). CONCLUSION Valsartan inhibits the reaction of inflammation, when myocardium is undergoing ischemia-reperfusion injury. IPC activates survival signaling of the myocardium by the phosphorylation of STAT3 and inhibits the reaction of myocardial inflammation. Valsartan can partly inhibit the activation of STAT3, and produce the role of myocardial protection.

参考文献/References

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备注/Memo

备注/Memo:
收稿日期：2007-11-19.基金项目：黑龙江省科技攻关课题项目资助（GC04C301） 通讯作者：寇俊杰，主任医师，博士，主要从事缺血/再灌注方面的研究Email:junjiekou@yahoo.com
更新日期/Last Update: 2009-04-02