Aim:To investigate the effects of epigallocatechin gallate(EGCG)on pressureoverload and hydrogen peroxide(H_2O_2)induced cardiac myocyte apoptosis.Methods:Cardiac hypertrophy was established in rats by abdominal aorticconstriction.EGCG 25,50 and 100 mg/kg were administered intragastrically(ig).Cultured newborn rat cardiomyocytes were preincubated with EGCG,and oxida-tive stress injury was induced by H_2O_2.Results:In cardiac hypertrophy inducedby AC in rats,relative to the model group,EGCG 25,50 and 100 mg/kg ig for 6weeks dose-dependently reduced systolic blood pressure(SBP)and heart weightindices,decreased malondialdehyde(MDA)content,and increased superoxidedismutase(SOD)and glutathione peroxidase(GSH-PX)activity,both in serumand in the myocardium.Also,treatment with EGCG 50 and 100 mg/kg markedlyimproved cardiac structure and inhibited fibrosis in HE and van Gieson(VG)stain,and reduced apoptotic myocytes in the hypertrophic myocardium detected byterminal transferase-mediated dUTP-biotin nick end-labeling(TUNEL)assay.Inthe Western blot analysis,EGCG significantly inhibited pressure overload-inducedp53 increase and bcl-2 decrease.In H_2O_2-induced cardiomyocyte injury,whenpreincubated with myocytes for 6-48 h,EGCG 12.5-200 mg/L increased cell viabil-ity determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide(MTT)assay.EGCG also attenuated H_2O_2-induced lactate dehydrogenase(LDH)release and MDA formation,Meanwhile,EGCG 50 and 100 mg/L significantlyinhibited the cardiomyocyte apoptotic rate in flow cytometry.Conclusion:EGCGinhibits cardiac myocyte apoptosis and oxidative stress in pressure overload in-duced cardiac hypertrophy.Also,EGCG prevented cardiomyocyte apoptosisfrom oxidative stress in vitro.The mechanism might be related to the inhibitoryeffects of EGCG on p53 induction and bcl-2 decrease. Aim: To investigate the effects of epigallocatechin gallate (EGCG) on pressure overload and hydrogen peroxide (H 2 O 2) induced cardiac myocyte apoptosis. Methods: Cardiac hypertrophy was established in rats by abdominal aorticconstriction. EGCG 25, 50 and 100 mg / kg were administered intragastrically ig). Cultured newborn rat cardiomyocytes were preincubated with EGCG, and oxida-tive stress injury was induced by H_2O_2.Results: In cardiac hypertrophy induced by AC in rats, relative to the model group, EGCG 25, 50 and 100 mg / kg ig for 6weeks dose-dependently reduced systolic blood pressure (SBP) and heart weightindices, decreased malondialdehyde (MDA) content, and increased superoxidedismutase (SOD) and glutathione peroxidase (GSH-PX) activity, both in serumand in the myocardium. Als, treatment with EGCG 50 and 100 mg / kg markedly processed cardiac structure and rendered fibrosis in HE and van Gieson (VG) stain, and reduced apoptotic myocytes in the hypertrophic myocardium detected byterminal transferase-mediated dUTP-bi otin nick end-labeling (TUNEL) assay. Inthe Western blot analysis, EGCG significantly inhibited pressure overload-inducedp53 increase and bcl-2 decrease.In H_2O_2-induced cardiomyocyte injury, whenpreincubated with myocytes for 6-48 h, EGCG 12.5-200 mg / L increased cell viabil-ity determined by 3- (4,5-dimethylthiazol-2-yl) -2,5-diphenyltetrazolium bromide (MTT) assay.EGCG also attenuated H 2 O 2 -induced lactate dehydrogenase (LDH) release and MDA formation, Meanwhile, EGCG 50 and 100 mg / L significantly inhibitor of the cardiomyocyte apoptotic rate in flow cytometry. Confluence: EGCG inhibitors of cardiac myocyte apoptosis and oxidative stress in pressure overload in-duced cardiac hypertrophy. Also, EGCG prevented cardiomyocyte apoptosis from oxidative stress in vitro. The mechanism might be related to the inhibitory effects of EGCG on p53 induction and bcl-2 decrease.