心肌康对慢性病毒性心肌炎小鼠心肌细胞凋亡及Fas/FasL蛋白表达影响的实验研究

Experimental study of the Effect of XinJiKang on Apoptosis and Fas/FasL Protein Expressions of Myocardium in Mice with Chronic Coxsackievirus B_3 Myocarditis

目的:观察心肌康对慢性病毒性心肌炎小鼠心肌细胞凋亡及Fas/FasL蛋白表达的影响,探讨心肌康的作用机制。方法:给Balb/c小鼠多次接种嗜鼠心肌柯萨奇B3病毒制作慢性VMC模型,首次感染病毒50天后将存活小鼠分为模型组、心肌康组及氯沙坦组,同时设正常对照组,分别予以相应药物干预30天,采用原位末端标记法(TUNEL)检测心肌细胞凋亡及免疫组化方法检测Fas/FasL蛋白表达。结果:正常组未见到心肌细胞凋亡,模型组心肌细胞凋亡,凋亡率较正常组显著增加(P<0.05),心肌康组和氯沙坦组凋亡率较模型组显著降低(P<0.05)。模型组Fas/FasL蛋白表达较正常组显著增多(P<0.01),心肌康组和氯沙坦组较模型组显著降低(P<0.01)。结论:心肌细胞凋亡参与了慢性病毒性心肌炎的发病,心肌康能够抑制VMC心肌细胞的凋亡,通过下调Fas/FasL蛋白表达,对心肌细胞起到保护作用。

Objective： Observe the affect of XinJiKang on apoptosis and Fas/FasL protein expressions of myocardium in Balb/c mice with chronic Coxsackievirus B3 myocarditis. Methods ：To prepare the chronic viral myocarditis of murine model by inocuating with 100TCID50 Coxsackievirus B3 ,they were devided into 3 groups at random,such as model group, XinJiKang group,losartan group. At the same time ,other group was normal group. Apoptosis was measured hy termninal transferase mediated DNA nike end labeling assay（TUNEL） and the expressions of Fas/FasL protein in myocardium were determined by immunohistochemistry. Results No apoptotic cardimyocytes were found in normal group. More apoptosis cells were found among cardiac muscles in model group than normal group（ P 〈 0. 05 ）. The ratio of TUNEL-positive cardimyocytes was much lower in XinJiKang group and losartan group than in model group（ P 〈 0.05）. Compared with normal group,the protein expressions of Fas/FasL were increased remarkably in model group（ P 〈0.01 ） ,the protein expressions of Fas/FasL in XinJiKang group and losartan group were much lower than in model group. Conclusion： Cardic muscle cells apoptosis took part in the development of CVB3 viral myocarditis, XinJiKang could inhibit apoptosis in myocardium by decreasing the expressions of Fas/Fas L proteinin myocardium.