Objective:To investigate the effects of schisandrin B on protein expression of AKT,mTOR,TGF-?1 and collagen I in angiotensin II-induced myocardial fibrosis.Methods:1-3 day SD rat heart was used in this study and hearts were digested with 0.1%type? collagenase digestion,then using the differential adherence method to isolated cultured cardiac fibroblasts.The myocardial fibroblasts were randomly divided into the control group,Ang ? group,Ang ?+Sch B low dose group(Sch B 2.5×10-5 mol·L-1),Ang ?+Sch B high dose group(Sch B 7.5×10-5mol·L-1)and Ang ?+rapamycin group.The protein expressions of AKT,mTOR,TGF-?1 and collagen I in cardiac fibroblasts were detected by Western blot and analyzed.Results:1.Compared with the control group,Ang ? 10-7 mol·L-1 group could stimulated myocardial fibroblasts to significantly decrease the expression of p-AKT(P<0.05);Compared with the Ang II group,schisandrin B(concentration of 2.5×10-5 mol·L-1?7.5×10-5mol·L-1)group could significantly increase the expression of p-AKT with a dose-dependent manner(P<0.05).2.Compared with the control group,Ang II 10-7 mol·L-1 group could significantly enhance the expression of p-mTOR,TGF-?1 and collagen I;Compared with the Ang ? group,schisandrin B(concentration of 2.5×10-5 mol L-1?7.5×10-5mol·L-1)group could significantly decrease the expression of p-mTOR,TGF-?1 and collagen I with a dose-dependent manner(P<0.05).3.Compared with the Ang ? 10-7mol·L-1 group,administration of rapamycin 1×10-8 mol·L-1 could significantly decrease the expression of p-mTOR,TGF-?1 and collagen I(P<0.05).Conclusion:1.Ang ? induces myocardial fibrosis by down-regulating p-AKT protein expression,up-regulating p-mTOR,TGF-?1 protein expression and collagen I synthesis.2.Schisandrin B could improve angiotensin ?-induced myocardial fibrosis by down-regulating p-mTOR and TGF-?1 protein expression,up-regulation p-AKT protein expression,and inhibiting collagen I synthesis.3.Rapamycin could inhibit the synthesis of collagen I by down-regulating the expression of p-mTOR and TGF-?1 protein,thereby inhibit myocardial fibrosis. |