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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 =2 0 )、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 ,West ernblotting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。MMP 9在心肌梗死后心室重塑过程中可能具有特殊的地位。
Objective To observe the changes of matrix metalloproteinase 2, 9 (MMP 2, 9) and tissue inhibitor of metalloproteinase 1 (TIMP 1) after myocardial infarction in rats. Methods The model of myocardial infarction was established by ligating the anterior descending coronary artery of SD rats. Divided into control group (n = 20), myocardial infarction group (group I, n = 48), the expression of MMP 2 and 9 protein after myocardial infarction was determined by zymography. West ernblotting further identified the enzyme digestion Attributes. Results The presence of inactive MMP 9 in normal myocardium. The MMP 2 protein level increased at 1 and 2 weeks after myocardial infarction, and the expression of MMP-2 protein increased. The MMP-1 activity increased at 1, 2 and 4 weeks of MMP-9 expression and the expression of TIMP-1 protein decreased. Conclusion Myocardial infarction myocardial MMP 9 activity increased and protein content increased, TIMP 1 protein content is reduced, is an important part of ventricular remodeling mechanism. MMP 9 may play a special role in the process of ventricular remodeling after myocardial infarction.