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目的研究辛伐他汀对盐酸异丙基肾上腺素(isoproterenol hydrochloride,Isp)所致心肌纤维化大鼠单核细胞趋化蛋白-1(MCP-1)表达及其巨噬细胞浸润的影响,探讨其抗纤维化的机制。方法应用注射Isp方法建立大鼠心肌缺血坏死模型,18只SD大鼠随机分为对照组、模型组和辛伐他汀组,每组6只。2周后Masson染色观察心肌间质胶原容积分数(CVF),免疫组化染色观察单核巨噬细胞抗原(ED1)数量,ELISA法和RT-PCR分别检测心肌MCP-1蛋白和mRNA的表达。结果模型组CVF、ED1阳性细胞数、MCP-1蛋白和MCP-1mRNA表达均高于对照组(P<0.01)。与模型组相比,辛伐他汀组CVF、ED1阳性细胞数、MCP-1蛋白和mRNA表达均降低(P<0.05或P<0.01),但仍高于对照组(P<0.05或P<0.01)。结论辛伐他汀可能通过降低MCP-1表达、减少巨噬细胞浸润发挥抗心肌纤维化作用。
Objective To investigate the effect of simvastatin on the expression of monocyte chemoattractant protein-1 (MCP-1) and its macrophage infiltration induced by isoproterenol hydrochloride (Isp) Anti-fibrosis mechanism. Methods The myocardial ischemic necrosis model was established by Isp injection. Eighteen SD rats were randomly divided into control group, model group and simvastatin group, with 6 rats in each group. After 2 weeks, the volume of myocardial interstitial collagen (CVF) was observed by Masson staining. The number of monocyte-macrophage antigen (ED1) was detected by immunohistochemistry. The expression of MCP-1 protein and mRNA were detected by ELISA and RT-PCR respectively. Results The expression of CVF, ED1 positive cells, MCP-1 protein and MCP-1 mRNA in model group were higher than those in control group (P <0.01). Compared with the model group, the expression of CVF, ED1 positive cells and MCP-1 protein and mRNA in Simvastatin group were significantly lower than those in the control group (P <0.05 or P <0.01) ). Conclusion Simvastatin may play an anti-myocardial fibrosis effect by decreasing the expression of MCP-1 and decreasing the infiltration of macrophages.