Protective effect of TGF-β-Smads signal-based oxymatrine on myocardial fibrosis induced by acute myocardial infarction in rats

Abstract

To study the protective effect of oxymatrine (OMT) on myocardial fibrosis induced by acute myocardial infarction in rats and its effect on TGF-beta-Smads signal pathway. Arteria coronaria ligation-induced acute myocardial infarction model was established in rats. The survived rats were randomly allotted into the model group, 50, 25, 12.5 mg x kg(-1) OMT groups, the 50 mg x kg(-1) captopril group, and the Sham-operated group which was treated as the model group without the arteria coranaria ligation. After 8 weeks of ligation, myocardial fibrosis was detected by HE and Masson staining, and the RT-PCR method were used to detect the expression of mRNA of TGF-beta-Smads signal system. The histopathological examination showed decrease in cardiocytes, deposition of extra-cellular matrix, and increase of collagen contents after 8 weeks of ligation. RT-PCR results showed that mRNA expressions of TGF-beta1, TbetaR1, Smad2, Smad3 and Smad4 significantly increased, but mRNA expression of Smad7 is remarkable lower than the sham-operated group. Treatment with OMT for 8 weeks could remarkably inhibit myocardial fibrosis, decrease mRNA expressions of TGF-beta1, TbetaR1, Smad2, Smad3, and Smad4, and increase mRNA expressions of Smad7. OMT has the inhibitory effect on the experimental myocardial fibrosis induced by AMI in rats. Its mechanism may be closely related to TGF-beta-Smads signal system.