OBJECTIVE： To study the inhibitory effects of Pseudostellaria heterophylla polysaccharide on myocardial apoptosis of ischemia-reperfusion injury （IRI） model rats， and to investigate its mechanism. METHODS： Totally 72 SD rats were selected and randomly divided into sham operation group， model group， positive drug group （Nifedipine tablets， 5 mg/kg） and P. heterophylla polysaccharide high-dose， medium-dose and low-dose groups （7.5， 15， 30 g/kg）， with 12 rats in each group. Sham operation group and model group were given water intragastrically， and other groups were given relevant medicine intragastrically for 7 d. The IRI model was established by ligating the anterior descending branch of left coronary artery， reperfusing 120 min after 30 min of myocardial ischemia （not occluded only in sham operation group）. HE staining was used to observe the pathological changes of myocardium in rats under microscope. Myocardial apoptosis was detected by TUNEL method. The protein expression levels of  Bax， Bcl-2 and Caspase-3 in myocardial tissue were detected by Western blot method. RESULTS： Compared with model group， pathological changes of myocardial tissue were relieved significantly in P. heterophylla polysaccharide groups， while the number of myocardial cell apoptosis was decreased significantly. The protein expression levels of Bax， the protein expression ratio of Bax and Bcl-2 in myocardial tissue were decreased significantly in P. heterophylla polysaccharide groups； those of Caspase-3 in P. heterophylla polysaccharide low-dose and medium-dose groups were decreased significantly； those of Bcl-2 were increased significantly in P. heterophylla polysaccharide high-dose group， with statistical significance（P＜0.05）. CONCLUSIONS： P. heterophylla polysaccharide can significantly relieve myocardial tissue injury and inhibit myocardial apoptosis in IRI model rats. Its mechanism may be associated with reducing proapoptotic protein Bax and Caspase-3 and raising apoptotic protein Bcl-2 expression.