Epigallocatechin gallate protects H9c2 cardiomyoblasts against hydrogen dioxides- induced apoptosis and telomere attrition

Epigallocatechin gallate (EGCG), the major component of polyphenols in green tea, has recently attracted considerable attention for its cardioprotective effects. Telomere signalling plays a role in regulating cardiomyocyte apoptosis during cardiac dysfunction. The purpose of this study was to investigate the effects of EGCG on oxidative stress-induced apoptosis and telomere attrition in cardiomyocytes. H9c2 cells were incubated with EGCG, 50 and 100 mg/l, for 24 h. Apoptosis induced by 200 μmol/l hydrogen dioxide (H2O2) was analyzed by DAPI nuclear staining, electron microscopy, electrophoresis of DNA fragments and flow cytometry. When H9c2 cells were incubated with H2O2 for 12–24 h, the intracellular and extracellular H2O2 concentrations were not affected by the presence of EGCG. Chromatin condensation, DNA fragmentation and apoptotic body formation were observed in H2O2-induced injury. Flow cytometry analysis showed that the apoptotic rate increased remarkably. EGCG significantly inhibited H2O2-induced apoptotic morphological changes and apoptotic rate. When H9c2 cells were incubated with H2O2, the telomere length shortened and the protein expression of telomere repeat-binding factor 2 (TRF2) decreased gradually, while the protein levels of p53 and p21 increased. EGCG significantly inhibited telomere attrition, TRF2 loss and p53, p21 upregulation induced by H2O2. These results suggested that EGCG might suppress oxidative stress-induced cardiomyocyte apoptosis through inhibiting telomere dependent apoptotic pathway.