Polyphenol epigallocatechin-3-gallate alleviates high Nucose high induced H9C2 cell damage through PI3K/Akt pathway

OBJECTIVE: The aim of this work was to study the protective effect of polyphenol epigallocatechin-3-gallate (EGCG) on high glucose-induced oxidative damage of H9C2 cells and to investigate the relationship between this effect and phosphatidyl inositol 3 kinase-serine/threonine kinase (P13K/Akt) signal transduction pathway. MATERIALS AND METHODS: H9C2 cells were used as objects of study, 350 mM glucose serum-free medium was used as the high glucose molding condition, and LY294002 (10 pM) was used as the P13K/Akt inhibitor. 3-(4,5-dimethylthiazol-2-y1)2,5-diphenyl tetrazolium bromide (MTT) assay was used to detect the cell viability, lactate dehydrogenase (LDH) assay was used to detect the cytotoxicity, flow cytometry was used to detect the proportion of cell apoptosis, and Western blotting was used to detect the expressions of cell-associated proteins. RESULTS: Cell viability was reduced and cell apoptosis was increased by 350 mM high glucose. The high glucose-induced apoptosis was alleviated and the Akt expression in cells was increased by EGCG. The protective effect of EGCG was reduced after inhibition of P13K/Akt pathway. CONCLUSIONS: EGCG protects H9C2 cells from high glucose-induced damage. EGCG plays the protective effect through inducing the P13K/Akt pathway activation.