Effect of hypericin on myocardial fibrosis of chronic viral myocarditis of mice and its mechanism / 中草药

ABSTRACT

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.