EGCG inhibits cardiomyocyte apoptosis in pressure overload-induced cardiac hypertrophy and protects cardiomyocytes from oxidative stress in rats
2007
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 aortic
constriction. EGCG 25, 50 and 100 mg/kg were administered intragastrically (ig).
Cultured newborn rat cardiomyocytes were preincubated with EGCG, and oxidative
stress injury was induced by H 2 O 2 . Results: In cardiac hypertrophy induced
by AC in rats, relative to the model group, EGCG 25, 50 and 100 mg/kg ig for 6
weeks dose-dependently reduced systolic blood pressure (SBP) and heart weight
indices, decreased malondialdehyde (MDA) content, and increased superoxide
dismutase (SOD) and glutathione peroxidase (GSH-PX) activity, both in serum
and in the myocardium. Also, treatment with EGCG 50 and 100 mg/kg markedly
improved cardiac structure and inhibited fibrosis in HE and van Gieson (VG) stain,
and reduced apoptotic myocytes in the hypertrophic myocardium detected by
terminal transferase-mediated dUTP-biotin nick end-labeling (TUNEL) assay. In
the Western blot analysis, EGCG significantly inhibited pressure overload-induced
p53 increase and bcl-2 decrease. In H 2 O 2 -induced cardiomyocyte injury, when
preincubated with myocytes for 6−48 h, EGCG 12.5−200 mg/L increased cell viability
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
inhibited the cardiomyocyte apoptotic rate in flow cytometry. Conclusion: EGCG
inhibits cardiac myocyte apoptosis and oxidative stress in pressure overload induced
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.
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