Study on mechanism of TGF-beta-Smad pathways in myocardial fibrosis(MF) of VMC chronic phase and captopril intervention

【Objective】 To investigate the mechanism of TGF-beta-SMAD pathway in myocardial fibrosis(MF) of VMC Chronic Phase and the intervention by captopril.【Methods】 50 balb/c rats were made VMC myocardial fibrosis model by intraperitoneal injection with coxsackie viruses B3 continuously through two mouth.And the other 10 as normal group were inoculated ip with EMEM solution without CVB3.The 40 model rats were divided into two group: the model group and the captopril group.The latter were treated by captopril every day and were made pathological section after the treatment after 45 days.Then observed the fibrosis degree by HE and Masson dyeing,detected the expression of TGF beta-1 by semi-quantitative RT-PCR and the expression of mouse myocardial Smad 2/3,Smad 7 protein determinated by immunohistochemical dyeing.【Results】 The infection cells appeared denaturization and necrosis,while little cells emerged inflammatory infiltrate.Fibrosis and calcification presented between the cells,in addition,myocardial collagen fibers increased significantly in masson dyeing cells.The expression of TGF beta-1 in captopril group increased than the normal group.And the Smad 2/3 in model group were higher as well the Smad 7 were lower(P 0.05).【Conclusion】 One of the mechanism that captopril restrain myocardial fibrosis in VMC chronic phase maybe by Blocking the TGF-beta-Smad signal transduction pathway.