Aim To explore the effect of Nrf2 gene in silent bone marrow mesenchymal stem cells （MSC） that take siRNA as the vector on the myocardial fibrosis and ventricular remodeling after the treatment of rat myocardial infarction （MI） with its transplantation as well as to investigate the potential mechanism of this process.Methods The established MI rat models were randomly divided into MSC transplantation group with silent Nrf2 gene （MSCNrf2－/－）,MSC transplantation group with over expression of Nrf2 gene （MSCNrf2＋/＋）,and MSC transplantation group with PBS （control group）,12 rats in each group. At the 28 th day after cell transplantation,the collagen deposition and fibrosis degrees after MI were evaluated using myocardial tissue Masson staining,the expression levels of infarcted myocardium Nrf2 and heme oxygenase-1 （HO-1） proteins were detected using Western blot,LVEDD,LVESD and LVEF were evaluated using echocardiography.Results At the 28 th day after cell transplantation,Masson staining results showed that myocardial tissue fibrosis degree in MSCNrf2－/－ group was severer than that in control group （P<0.05）,but the MSCNrf2＋/＋group showed to decrease with control group （P<0.05）. Western blot results showed that the Nrf2 and HO-1 protein expression decreased in MSCNrf2－/－ group with a statistically significant difference compared with control group （P<0.05）,however,the Nrf2 and HO-1 protein expression in MSCNrf2＋/＋ group significantly increased compared with control group （P<0.05）. Echocardiography results showed that LVEDD and LVESD values increased and LVEF value decreased in MSCNrf2－/－ group with a statistically significant difference compared with control group （P<0.05）. While the comparison of control group,LVEDD and LVESD values decreased and LVEF value increased in MSCNrf2＋/＋ group.Conclusions Nrf2 siRNA can effectively interfere the expression of Nrf2 in MSC and reduce the repair ability of exogenous MSC for MI heart,which will increase the collagen deposition in infarcted area,thus contributing to ventricular remodeling and reducing cardiac function.