替米沙坦对心肌梗死大鼠心肌重构基质金属蛋白酶表达水平的影响

目的证实替米沙坦对心肌梗死大鼠基质金属蛋白酶(MMPs)和心室重构的影响。方法结扎SD大鼠冠状动脉前降支做心肌梗死大鼠模型后,随机分为心肌梗死组15只、替米沙坦组15只,另SD大鼠开胸未结扎前降支作为对照组10只,3组均予正常饮食,其中替米沙坦组心肌梗死后予连续用药(替米沙坦3 mg.kg-1.d-1灌胃)2周。各组随机抽取5只大鼠,取梗死心肌标本组织进行苏木素-伊红(HE)染色病理检查,SABC法做MMP-2、MMP-9、心肌胶原纤维成分胶原(collagen)Ⅰc、ollagenⅢ、金属蛋白抑制因子(TIMP)-1免疫组织化学染色3,3-二氨基联苯胺(DAB)显色,用平均吸光度(A值)测定来计算MMP-2、MMP-9、collagenⅠc、ollagenⅢ、TIMP-1的表达水平,并做统计分析。结果与对照组比较,心肌梗死模型的两组大鼠间质胶原纤维增多,MMP-2、MMP-9、TIMP-1活性显著增高;替米沙坦干预组与心肌梗死组比较,间质内胶原明显减少,MMP-2、MMP-9、TIMP-1水平显著降低。结论替米沙坦可抑制大鼠心肌梗死后MMP-2、MMP-9的活性,使胶原含量和Ⅰ/Ⅲ胶原比例降低,对心肌梗死后大鼠的心室重构有改善作用。

Effect of telmisartan on matrix metalloproteinase expression in myocardial infarction rats

ObjectiveTo investigate the effect of telmisartan on ventricular remodeling and matrix metalloproteinase in acute myocardial infarction rats.MethodsMale SD rats were randomly divided into AMI group,telmisartan treatment group and control group.The AMI model was established by ligation of coronary artery.It was estimated success through rising of the ST-Segment in electrocardiogram.Telmisartan treatment group rats were treated with telmisartan(3 mg·kg-1·d-1) after MI.Statistical analysis was performed by analysis of SPSS 10.0 system.ResultsCompared with control group MMP-2,MMP-9,collagenⅠ,Ⅲ and TIMP-1 in AMI group and telmisartan treatment group were significantly higher than that in control group (P<0.05).While the level of telmisartan treatment group were significantly lower than that of AMI group(P<0.05).ConclusionTelmisartan improves ventricular remodeling in acute myocardial infaction rats.Telmisartan therapy makes the level of collagen and the proportion of collagenⅠ and collagen Ⅲ drop and the expression of MMP-2 and MMP-9 decrease,which prove that it has a magnificent effect on myocardial remodeling in acute myocardial infaction rats.