目的 观察金丝桃素对病毒性心肌炎小鼠慢性期心肌纤维化形成的影响及JAK/STAT传导通路在其中作用。方法60 只雄性Balb/c小鼠采用间断、多次ip柯萨奇病毒B₃的方法制备病毒性心肌炎心肌纤维化模型。另选10只雄性小鼠作为对照组。模型制备成功后，存活的小鼠随机分为4组，即模型组，金丝桃素高和低剂量（50、15 mg/kg）组，卡托普利（50 mg/kg）组，每日ig给药1次，连续给药30 d。ELISA法检测血清中I型、III型胶原水平；半定量RT-PCR法和免疫组化法检测JAK1/STAT3表达；左心室行Masson染色，进行心肌组织学观察。结果 模型组小鼠血清中I型、III型胶原水平明显升高；JAK1与STAT3基因表达上调，与对照组相比差异显著（P＜0.05）。金丝桃素及卡托普利组均能够明显降低小鼠血清中I型、III型胶原水平，下调JAK1/STAT3表达；心肌组织病理学观察可见小鼠心肌纤维化程度得到改善，与模型组比较差异显著（P＜0.05）。结论 在病毒性心肌炎慢性期心肌纤维化过程中，JAK1/STAT3传导通路的激活可能是心肌组织I型、III型胶原表达增强进而形成心肌纤维化的机制之一；而金丝桃素可通过阻断JAK1/STAT3传导通路，抑制病毒性心肌炎慢性期心肌纤维化。

Objective To investigate the role of JAK/STAT signal pathway in myocardial fibrosis (MF) of the chronic viral myocarditis (VMC) of mice and hypericin intervention study. Methods Sixty healthy male Balb/c mice were used to establish the MF model by intermittent multiple ip injection of coxsackie B₃, another 10 mice were used as normal control. Two months after the modeling, survival mice were randomly divided into four groups, model group, low- or high-dose hypericin group, and Captopril group. The mice were treated by Captopril or hypericin, respectively, ig administration, once a day. After 30 d, we took the myocardium of left ventricle to dye with Masson, to observe the cardiac histological changes. The serum type I collagen and type III collagen were detected by the means of ELISA, and the expression of JAK1 and STAT3 was observed with semi-quantitative RT-PCR and immunohistochemistry technique. Results The model group, serum type I and type III collagen increased significantly, the expression level of JAK1/STAT3 was higher than that of the normal group, and the difference was significant (P < 0.05). While the hypericin and Captopril treatment could significantly reduce serum expression of type I and, type III collagen, and decrease JAK1/STAT3 expression. Histology showed the improvement of myocardial fibrosis degree, and a significant difference was observed when comparing with the model group (P < 0.05). Conclusion In the process of chronic viral myocarditis, the activation of JAK1/STAT3 pathway may be one of pathological mechanisms of the MF-induced with type I and type III collagen increasing. Hypericin could inhibit the myocardial fibrosis by blocking JAK1/STAT3 pathway.