OBJECTIVE To investigate the protective effect of paeoniflorin(PF)on cardiac dysfunction and myocardial cell injury induced by cisplatin(CDDP)in rats.METHODS SD male rats were randomly divided into control group,CPPD group,and CDDP PF+low-dose,high-dose group.PowerLab multifunctional recorder was used to detect the related indexes of cardiac function:the changes of left ventricular peak pressure(LVSP),left ventricular end-diastolic pressure(LVEDP)and left ventricular pressure change rate(±dp/dt).Serum levels of inflammatory factors TNF-α,IL-1β and IL-6 were measured in each group.Myocardial tissue was stained to observe the changes of tissue structure.H9c2 cardiomyocytes were divided into control group,CDDP group,PF group and CDDP+PF group.The activity of H9c2 cardiomyocytes was measured by CCK-8.The apoptosis of cardiomyocytes in each group was detected by flow cytometry.The expressions of MAPK signaling pathway related proteins p38,ERK,JNK and their phosphorylated proteins and apoptosis-related proteins Bax,Bcl-2,Casp3,Cl-casp3 were detected in cardiomyocytes by Western blotting.RESULTS Compared with the control group,LVSP and±dp/dt decreased,LVEDP increased in rats of CDDP group(P<0.01).Compared with CDDP group,both CDDP+low-dose and high-dose PF pretreatment increased LVSP and±dp/dt value(P<0.05 or P<0.01),decreased LVEDP(P<0.01),and could decrease the serum inflammatory factor TNF-α,IL-1β and IL-6(P<0.01).Cell level results showed that compared with control group,in CDDP group,the cell activity decreased,the apoptosis-related protein Bax,Cl-casp3 increased(P<0.01),expression of anti-apoptotic protein Bcl-2 decreased(P<0.01),and the expression of p38 and ERK phosphorylation also increased(P<0.01).Compared with CDDP group,PF could restore cell activit,down-regulate apoptosis-related protein Bax,Cl-casp3(P<0.05 or P<0.01),and increase anti-apoptotic protein Bcl-2 expression(P<0.01),inhibit MAPK pathway p38 and ERK phosphorylation expression(P<0.01).CONCLUSION PF can restore cardiac dysfunction and myocardial cell injury induced by cisplatin in rats,which may be related to inhibiting inflammation and apoptosis by regulating ERK/p38 MAPK signal expression.