Objective:To explore the effects of Panax Quinquefolium Saponin(PQS) on phosphatidylinositol3-kinase/serine threonine kinase(PI3K/Akt) pathway of neonatal rat myocardial cells subjected to hypoxia.Methods:Neonatal rat myocardial cells were cultured in vitro.After the myocardial cell injury was induced by hypoxia,the cells were randomized into 5 groups:the normal group,the model group,the positive control group(Ciclosporin A,2 μ mol/L),the low-dose PQS group(PQSL,25mg/L),and the high-dose PQS group(PQSH,50 mg/L).Morphology and behavior of myocardial cells were observed under an inverted microscope.Apoptosis rate and lactate dehydrogenase(LDH) leakage rate of myocardial cells were determined by colorimetry.Mitochondrial transmembrane potential was assessed using a fiuorexon laser.Phospho-glycogen synthase kinase(GSK)-3 β and phospho-Akt as well as cytochrome C were determined by Western blot.Results:LDH leakage in the Ciclosporin A group,PQSH group and PQSL group reduced progressively compared with the model group(P<0.05).Akt and GSK-3 β was strongly phosphorylated after treatment with Ciclosporin A and PQS compared with the model group(P<0.05,P<0.01).Compared with the model group(16.41 ±1.74;35.28 ±6.30),both the integrated optical density of mitochondrial permeability transition pore(MPTP) and the mitochondrial transmembrane potential significantly increased in the PQSH group(42.74 + 2.12;71.36 ±6.54) and the PQSL group(39.58 ±1.49;66.99 ±5.45;P<0.05,P<0.01).However,the protein of cytochrome C outside the mitochondrion decreased in the PQSH group(273.66 ±14.61) and the PQSL group(259.62 ±17.31) compared with the model group(502.41 ±17.76;P<0.05).Conclusion:Through activation of the PI3K/AW pathway and inhibition of the MPTP,PQS might protect the heart against ischemia injury and apoptosis of myocardial cells. Objective: To explore the effects of Panax Quinquefolium Saponin (PQS) on phosphatidylinositol 3-kinase / serine threonine kinase (PI3K / Akt) pathway of neonatal rat myocardial cells subjected to hypoxia. Methods: Neonatal rat myocardial cells were cultured in vitro. After the myocardial infarction cell injury was induced by hypoxia, the cells were randomized into 5 groups: the normal group, the model group, the positive control group (Ciclosporin A, 2 μ mol / L), the low-dose PQS group (PQSL, 25 mg / L ) and the high-dose PQS group (PQSH, 50 mg / L). Morphology and behavior of myocardial cells were observed under an inverted microscope. Apoptosis rate and lactate dehydrogenase (LDH) leakage rate of myocardial cells were determined by colorimetry. Mitochondrial Phospho-Akt as well as cytochrome C were determined by Western blot. Results: LDH leakage in the Ciclosporin A group, PQSH group and PQSL group reduced progressively compared with the model group (P <0.05, P <0.05) .Akt and GSK-3β were strongly phosphorylated after treatment with Ciclosporin A and PQS compared with the model group 1.74; 35.28 ± 6.30), both the integrated optical density of mitochondrial permeability transition pore (MPTP) and the mitochondrial transmembrane potential significantly increased in the PQSH group (42.74 + 2.12; 71.36 ± 6.54) and the PQSL group (39.58 ± 1.49; 66.99 P <0.05, P <0.01) .Wowever, the protein of cytochrome C outside the mitochondrion decreased in the PQSH group (273.66 ± 14.61) and the PQSL group (259.62 ± 17.31) compared with the model group (502.41 ± 17.76 ; P <0.05) .Conclusion: Through activation of the PI3K / AW pathway and inhibition of the MPTP, PQS might protect the heart against ischemia injury and apoptosis of myocardial cells.