Inhibitory Effect and Mechanism of Paeoniflorin on Isoproterenol-induced Myocardial Hypertrophy in Rats

Objective: To investigate the inhibitory effect of paeoniflorin on isoproterenol( ISO)-induced myocardial hypertrophy in rats and its potential mechanism. Method: Totally 40 SD rats were randomly divided into five groups: the normal group,the model group and paeoniflorin low,middle and high does groups( 20,40,80 mg·kg- 1),with eight rats in each group. Except for the normal group,all of the rest groups were subcutaneously injected with isoprenaline( 5 mg·kg- 1) for 10 days to induce the myocardial hypertrophy model and at the same time intraperitoneally injected with PEF. At the end of drugs treatment,their hearts were collected to measure the heart weight( HW),left ventricular weight( LVW) and the ratio to body weight( BW). The changes in the size of cardiac cells were observed by hematoxylin-eosin staining. The mRNA expressions of atrial natriuretic peptide( ANP),brain natriuretic peptide( BNP) and cardiotrophin-1( CT-1) were measured by real-time PCR. The protein expression of CT-1 and level of reactive oxygen species( ROS) in myocardium were detected by Western blot and DCFH-DA florescent probe,respectively. Result: Compared with the normal group,the model group showed significant increases in the ratio of HW / BW and LVW / BW,cardiac myocyte cross-sectional area,mRNA expressions of ANP and BNP,CT-1 mRNA and protein expressions and ROS level at myocardial tissues( P <0. 01). Compared with the model group,PEF could obviously decrease the ratio of HW / BW and LVW / BW,cardiac myocyte cross-sectional area,mRNA expressions of ANP and BNP,CT-1 mRNA and protein expressions and ROS level at myocardial tissues. Conclusion: PEF can inhibit ISO-induced myocardial hypertrophy. Its mechanism may be correlated with the down-regulation of CT-1 expression by inhibiting ROS production.