Abstract: Objective: To observe the improvement effect of panax notoginseng saponins on the cardiac function of the rats with chronic heart failure(CHF), and to investigate the possible mechanism. Methods: Abdominal aortic constriction was used to establish the CHF rat models. Sixty model rats were randomly divided into model group, positive control group, low, medium and high doses of panax notoginseng saponins groups (n=12).Another 12 rats were taken as sham operation group. Color doppler ultrasound was used to detect the left ventricular end-diastolic diameter (LVEDD), left ventricular end-systolic diameter (LVESD), left ventricular posterior wall diastolic thickness (LVPWD), left ventricular ejection fraction (LVEF), cardiac output (CO), left ventricular end-diastolic pressure (LVEDP), left ventricular systolic pressure (LVSP), maximal rate of increase of left ventricular pressure(+dp/dt max) and maximal rate of decrease of left ventricular pressure(-dp/dt max) of the rats in various groups,HE staining was used to observe the pathomorphology of myocardium tissue of the rats in various groups,TUNEL method was used to detect the apoptotic rates of cadiomyocytes of the rats in various groups,and Western blotting method was used to detect the expression levels of extracellular signal-regulated kinase(ERK),phosphorylation ERK (p-ERK),c-Jun NH2-terminal protein kinase(JNK),phosphorylation JNK(p-JNK),p38, and p-p38 proteins in myocardium tissue of the rats in various groups. ELISA was used to determine the serum levels of tumor necrosis factor-α(TNF-α) and interleukin-6(IL-6) of the rats in various groups. Results: Compared with sham operation group, the LVEDD, LVESD, LVPWD, LVEDP and -dp/dt max of the rats in model group were significantly increased(P<0.05), while the LVEF, CO, LVSP, and +dp/dt max were significantly decreased(P<0.05). Compared with model group, the LVEDD, LVESD, LVPWD, LVEDP and -dp/dt max of the rats in positive control group and low, medium and high doses of panax notoginseng saponins groups were significantly decreased(P<0.05), while the LVEF, CO, LVSP and +dp/dt max were significantly increased (P<0.05).The cardiomyocytes of the rats in model group were hypertrophy and necrosis, and the myocardial fibers were irregular arrangement, with inflammatory cell infiltration and myocardial cell apoptosis. The structure of myocardium tissue of the rats in positive control group and low, medium and high doses of panax notoginseng saponins groups were nearly complete, the cardiomyocyte hypertrophy was relieved, and the myocardial fibers were slagking. Compared with sham operation group, the apoptotic rate of cardiomyocytes of the rats in model group was significantly decreased(P<0.05), the expression levels of p-ERK,p-JNK,and p-p38 proteins in myocardium tissue of the rats in model group were significantly increased(P<0.05), the serum levels of TNF-α and IL-6 of the rats in model group were significantly increased (P<0.05).Compared with model group, the apoptotic rates of cardiomyocytes of the rats in positive control group and low, medium and high doses of panax notoginseng saponins groups were significantly decreased(P<0.05), the expression levels of p-ERK,p-JNK,p-p38 proteins in myocardial tissue were significantly decreased (P<0.05), and the serum levels of TNF-α and IL-6 were significantly decreased(P<0.05). Conclusion: Panax notoginseng saponins can inhibit the apoptosis of the cardiomyocytes and improve the CHF by down-regulating the expression levels of p-ERK,p-JNK and p-p38 proteins and inhibiting the secretion of serum inflammatory factors.

Key words: panax notoginseng saponins, heart failure, cardiac function, MAPK signaling pathway, inflammatory cytokine