Objective: To investigate the role of Rho/Rock signal transduction pathway in the myocardial fibrosis(MF)in chronic phase viral myocarditis mice

and to study the therapeutic mechanism of Sanshen decoction(SD). Method: Hundred and twenty BALB/c rats were inoculated ip with diluted coxsackievirus B3(CVB3) EMEM solution fortnightly interval to establish the model of viral myocarditis(VMC) with MF. The survival model mice were randomized into 5 groups:model group

captopril group

high-

middle-and low-dosage SD groups. All the ras were treated by infusing the stomach with the medicine.The therapeutic dose of SD groups was respectively 3

2

1 g·kg-1

and the captopril group was 45 mg·kg-1

the model group and normal group were given the equivalence saline by gavage.Then N-terminal procollagen Ⅰ propeptide(PⅠNP) and N-terminal procollagen Ⅲ propeptide(PⅢNP) were detected by the means of enzyme-linked immunosorbant assay(ELISA)

and the gene expression of Rock1 was detected by RT-PCR

and the content of angiotensin Ⅱ(Ang Ⅱ) in serum by radioimmunoassay. Result: SD could decrease PⅠNP and PⅢNP obviously(P<0.05)

compared with the normal group. The expression levels of Rho/Rock signal pathway were higher than normal group(P<0.05)in the chronic phase of VMC. The contents of Ang Ⅱ in serum in model group were higher than the normal group(P<0.05). Conclusion: The activation of Rho/Rock signal transduction pathway is one of the mechanism of the CFBs proliferation and collagen synthesis stimulated by Ang Ⅱ in myocardial fibrosis of VMC. Sanshen decoction can inhibit the restrain myocardial fibrosis by blocking the signal pathway.