EGCG inhibits cardiomyocyte apoptosis in pressure overload-induced cardiac hypertrophy and protects cardiomyocytes from oxidative stress in rats

Aim:To investigate the effects of epigallocatechin gallate(EGCG)on pressureoverload and hydrogen peroxide(H2O2)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 H2O2.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 H2O2-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 H2O2-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.