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目的探讨基质金属蛋白酶鄄1(MMP鄄1)、金属蛋白酶组织抑制因子鄄1(TIMP鄄1)在心肌炎小鼠心肌胶原重构中的作用。方法用VG染色和图像分析、原位杂交方法观察病毒性心肌炎小鼠及同龄的对照小鼠各时期心肌组织胶原改变及MMP鄄1mRNA、TIMP鄄1mRNA的表达。结果与对照组比较,感染后第14天心肌组织胶原增加不明显,感染后第28天心肌组织血管周围胶原面积(PVCA)显著增加(P<0.001),感染后第56天PVCA及心肌胶原容积分数(CVF)均显著增加(P<0.001)。感染后第7天心肌MMP鄄1mRNA呈现一过性表达;感染后第7天可见TIMP鄄1mRNA表达,第14～21天最为明显,此后减弱,直到第56天。结论TIMP鄄1mRNA表达上调可能在病毒性心肌炎心肌胶原重构中起着重要作用。
Objective To investigate the role of matrix metalloproteinase-1 (MMP-1) and tissue inhibitor of metalloproteinase-1 (TIMP-1) in cardiac myocyte remodeling in myocarditis mice. Methods VG staining, image analysis and in situ hybridization were used to observe the changes of collagen and MMP-1 mRNA and TIMP-1 mRNA expression in myocardium of myocarditis and myocarditis in mice of the same age. Results Compared with the control group, the increase of collagen in myocardium was not obvious on the 14th day after infection, and the perivascular collagen area (PVCA) increased significantly (P <0.001) on the 28th day after infection. On the 56th day after infection, PVCA and myocardial collagen volume The scores (CVF) increased significantly (P <0.001). On the 7th day after infection, the expression of MMP-1 mRNA in myocardium was transiently expressed. The expression of TIMP-1 mRNA was observed on the 7th day after infection, the most obvious on the 14th to 21st days, and then weakened until the 56th day. Conclusion Upregulation of TIMP-1 mRNA may play an important role in myocardial collagen remodeling in viral myocarditis.