心室重塑中基质金属蛋白酶和组织抑制酶的表达

目的 观察大鼠心肌梗死后基质金属蛋白酶-2，9(MMP-2，9)和组织金属蛋白酶抑制剂-1(TIMP-1)的变化规律。方法 结扎SD大鼠冠状动脉前降支建立心肌梗死模型。分为对照组(n=20)、心肌梗死组(Ⅰ组，n=48)，酶谱法测定心肌梗死后MMP-2，9活性蛋白的表达规律，Western blotting进一步确定所消化条带酶的属性。结果正常心肌中无活性MMP-9的存在。MMP-2蛋白水平在心肌梗死后第1、2周活性增强、表达增加，MMP-9第1、2、4周活性增强、表达增加，TIMP-1蛋白含量减少。结论 心肌梗死后心肌组织内MMP-2，9的活性增高和蛋白含量增加，TIMP-1蛋白含量减少，是心室重塑机制重要组成部分。MM-9在心肌梗死后心室重塑过程中可能具有特殊的地位。

Effects of matrix metalloproteinase on ventricular remodeling after myocardial infarction in rats

Objective To characterize the time-course of matrix metalloproteinase (MMP-2,9) and endogenous tissue inhibitor of MMPs (TIMP-1) up-regulation during left ventricular remodeling following myocardial infarction in rats.Methods The descending left coronary artery of male rats (Sprague-Dawley) was ligated to produce a myocardial infarction model.Sixty-eight rats were randomly divided into control group (n=20) and myocardial infarction group (n=48).Protein was obtained on left ventricular samples containing scar and myocardium together.The activity of MMPs was measured by zymography and determined by Western-blotting.Results The activities of MMP-9 were not detected in normal rat heart.The activities and amount of MMP-2 in the myocardial infarction group were increased significantly at the 1st and 2nd week,and MMP-9 at the 1st,2nd and 4th week.On the contrary,TIMP-1 protein was decreased.Conclusion After myocardial infarction,MMP-2,9 protein was increased significantly,while TIMP-1 protein was decreased.These changes may be the major causes of ventricular remodeling.MMP-9 may be crucial in the process of ventricular remodeling.