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|本期目录/Table of Contents|

血管紧张素Ⅱ受体拮抗剂对梗死心肌肌腱蛋白分布的影响(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2007年第6期
页码:
631-634
栏目:
基础研究
出版日期:
2007-12-20

文章信息/Info

Title:
Effect of angiotensionⅡon tenascinc in infarcted rat heart
作者:
杨大春; 杨永健; 张鑫; 宣兵
成都军区总医院心血管内科，四川 成都 610083
Author(s):
YANG Da-chun;  YANG Yong-jian;  ZHANG Xin;  XUAN Bing
Department of Cardiology, PLA General Hospital, Chengdu Military Area Comman, Chengdu 610083, Sichuan, China
关键词:
心肌梗死;  肾素血管紧张素Ⅱ; 受体;  基质金属蛋白酶;  肌腱蛋白
Keywords:
myocardial infarction;  angiotensionⅡ; receptors;  matrix metalloproteinases;  tenascin-c
分类号:
R541.2
DOI:
-
文献标识码:
A
摘要:
目的 探讨血管紧张素Ⅱ(AngⅡ)受体（AT1 ,AT2）拮抗剂对梗死心肌基质金属蛋白酶(MMPs)及细胞外基质肌腱蛋白（tenascin-c,TN-C）的调节作用。方法 结扎大鼠左冠状动脉建立心肌梗死模型，术前7 d起分别用安慰剂、AT1受体拮抗剂缬沙坦10 mg/（kg·d）、AT2受体拮抗剂PD123319 30 mg/（kg·d）。术后7 d放免法检测左心室游离壁（LVFW）、室间隔（IS）心肌组织基质金属蛋白酶MMP2，3，9、基质金属蛋白酶组织抑制物1（TIMP-1）的表达，免疫荧光检测LVFW、IS、RV心肌TNC的分布。结果 与假手术组相比，术后7 d手术组、缬沙坦组及PD123319组 IS和LVFW的 MMP2,3,9水平显著增加，TIMP-1水平显著减少（P<0.01）； TN-C在RV心肌组织及假手术组中不表达，在手术组和PD123319组IS和LVFW中表达增强，缬沙坦组表达较弱。 结论 AngⅡ参与梗死心肌组织的重构，通过AT1作用于MMPs，调节细胞外基质TN-C等，AT1受体拮抗剂的心脏保护作用与其抑制MMPs及TN-C有关。
Abstract:
AIM To investigate the effect of angiotensionⅡ(AngⅡ) receptors (AT1, AT2) antagonists on matrix metalloproteinases (MMPs) and tenascinc (TNC) in infarcted heart of rats. METHODS Rat myocardium infarction (MI) model was established by permanent ligation of the left coronary artery. The infarcted rats were treated respectively with placebo, valsartan (AT1 receptor antagonist, 10 mg/kg·d) or PD123319 (AT2 receptor antagonist, 30 mg/kg·d), beginning 7days before induction of myocardial infarction. On the 7th day after MI, the levels of MMP2,3,9, tissue inhibitors of matrix metalloproteinase1 (TIMP1) were determined by radio immunoassay (RIA) in left ventricular free wall (LVFW) and interventricular septum (IS). TNC distribution was also assayed by immunoflorescence. RESULTS In operation, Valsartan and PD123319 group, the levels of MMP2,3,9 increased in IS and LVFW, whereas the levels of TIMP1 decreased, with a significant difference from those in sham group (P<0.01). There was no expression of TNC in right cardiac ventricle (RV) and sham groups. TNC increased in operation and PD123319 groups while decreased in Valsartan group. CONCLUSION AngⅡ is involved in myocardial remodeling in infarcted heart by adjusting MMPs and TNC via AT1 receptor. The protective effect of AT1 receptor antagonists on the heart may be related to the inhibition of MMPs and TNC.

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备注/Memo

备注/Memo:
收稿日期：2006-08-18.作者简介：杨大春，主治医师，硕士 Email：yangdc71@163.com
更新日期/Last Update: