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目的：研究雷公藤甲素对柯萨奇病毒B3 病毒（CVB3）感染的病毒性心肌炎小鼠心肌细胞凋亡和Fas/FasL 蛋白表达的抑制作用，探讨TP 治疗病毒性心肌炎的作用机制。方法：将Balb/c 小鼠随机分成4 组作为动物模型，分别为对照组、模型组、利巴韦林组和TP 组。对照组腹腔注射生理盐水，其余三组腹腔注射CVB3，利巴韦林组和TP 组小鼠分别予以相应的药物治疗后，测定各组小鼠存活率及心肌病变积分，采用末端转移酶标记技术（TUNEL 法）检测小鼠心肌细胞凋亡，免疫组化法检测Fas/FasL 蛋白阳性表达。结果：空白对照组心肌无病变，利巴韦林组、TP 组与模型组相比有显著性差异（P <0.01）。正常组鲜见心肌细胞凋亡，模型组细胞凋亡率较正常组显著增加(P <0.01)，治疗组利巴韦林组和TP 组凋亡率比模型组明显降低(P<0.05, P<0.01)。模型组 Fas/FasL 表达比正常组显著增多(P <0.01)，治疗组利巴韦林组和TP 组较模型组显著降低(P <0.01)。结论：雷公藤甲素具有通过抑制Fas/FasL 蛋白的表达，减缓心肌细胞凋亡，达到抑制病毒性心肌炎从而保护心肌细胞的作用。

英文摘要:

Objective: To explore the effects of triptolide on apoptosis and expression of Fas/FasL in myocardial cells of mice with Coxsackievirus B3(CVB3) infected viral myocarditis. Methods: The Balb/c mice were randomly divided into four groups as animal models, namely the control group, model group, ribavirin group and TP group. Control group were injected intraperitoneally with normal saline, and other three groups were injected of CVB3. After treatment of ribavirin group and TP group, the survival rate of mice and myocardial histopathologic scores were determined. Terminal transferase labeling(TUNEL method) was used to detect mouse cardiomyocyte apoptosis, and immunohistochemistry to detect expression of Fas/FasL. Results: Cardiomyopathy of ribavirin group and TP group were significantly different compared with the model group (P <0.01). Compared with normal group, apoptosis rate of the model group was significantly increased (P <0.01). Apoptosis rate of ribavirin treatment group and TP group rate was significantly lower than model group (P <0.05, P <0.01). Expression of Fas/FasL in model group was significantly increased than the control group (P <0.01), and ribavirin treatment group and TP group was significantly lower than model group (P <0.01). Conclusion: Triptolide could inhibit apoptosis of cardiocytes through regulating the expression of Fas/FasL in order to inhibit viral myocarditis and protect myocardial cells.

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