大鼠急性心肌梗死后心肌局部CC亚族趋化因子mRNA的表达

Alteration of CC chemokines mRNA expression in cardiac tissue after acute myocardial infarction in rats

目的:研究急性心肌梗死(AMI)大鼠心肌局部CC亚族趋化因子———正常T细胞表达和分泌、活化时表 达下降的因子(RANTES)和巨噬细胞炎性蛋白 1α(MIP 1α)的表达,探讨AMI后T细胞浸润心肌组织的机制。方 法:在体结扎Wistar大鼠冠状动脉左前降支,建立AMI大鼠模型和假手术(SH)组对照,观察2组大鼠心肌局部病 理变化及血流动力学的变化。用半定量RT PCR方法分析AMI大鼠心肌梗死后1d,3d,1周,2周,8周心肌梗死 区和非梗死区趋化因子RANTES、MIP 1α的mRNA表达,HE染色切片观察淋巴细胞浸润。结果:①术后1周末,与 假手术组相比,AMI组大鼠左室腔扩大,室壁变薄;AMI大鼠心脏梗死区和非梗死区均可见淋巴细胞浸润,梗死区1 周最多((81.0±10.3)个/HP),非梗死区2周最多(19.0±8.2个/HP)。②与SH组比较,AMI组大鼠pLVED明显增 高,pLVS和+dp/dtmax显著降低(P<0.01)。③心肌梗死区和非梗死区趋化因子RANTES、MIP 1α的mRNA表达于 术后3d开始升高(梗死区RANTES为0.61±0.13,MIP 1α为1.32±0.09;非梗死区RANTES为0.31±0.14,MIP 1α为0.46±0.13),1周达峰值(梗死区RANTES为0.83±0.10,MIP 1α为2.03±0.10;非梗死区RANTES为 0.42±0.12,MIP 1α为1.32±0.09),其后开始下降,8周降至正常(梗死区RANTES为0.

Aim: To explore the infiltration mechanism of T cells after acute myocardial infarction (AMI) by examining the expression of macrophage inflammatory protein-1 alpha (MIP-1α) and the chemokine regulated on activation, normal T cell expressed and secreted (RANTES) in cardiac myocytes. Methods: Wistar rats were ligated left anterior descending branch in vivo to establish AMI model. The expression of chemokine and their receptors mRNA were analyzed using RT-PCR, and take count of the number of lymphocytes infiltrated in the infarcted region and remote zones. The sham operation group served as controls. Results: MIP-1α and RANTES mRNA increased at the 3rd day and reached the peak at 1 week in the infarcted region and remote zones, then decreased, and were not detected at 8 weeks. Lymphocytes were maximum at 1 week in the infarcted region but 2 weeks in remote zones. Conclusion: MIP-1α and RANTES increase in the heart of rats after AMI,which may induce lymphocyte infiltration.