Epigallocatechin‑3‑gallate protects from high glucose induced podocyte apoptosis via suppressing endoplasmic reticulum stress.

Podocytes serve a critical role in the development of many glomerular diseases, including diabetic nephropathy (DN). Epigallocatechin‑3‑gallate (EGCG), a predominant polyphenolic component of green tea, has indicated its therapeutic effects in diabetes. In the present study, mouse podocyte cells were cultured in vitro, cell injury was induced by high glucose, and the protective effect of EGCG on cell proliferation and apoptosis and the underlying mechanisms were investigated. The results demonstrated that high glucose significantly inhibited cell proliferation after 48 and 72 h compared with normal glucose and mannitol treatment. EGCG (20 µmol/l) markedly promoted podocyte proliferation after 24, 48 and 72 h incubation with high glucose. Furthermore, high glucose significantly reduced WT‑1 and nephrin expression in podocytes compared with the normal glucose and mannitol groups, while EGCG (20 µmol/l) treatment largely restored their expression. High glucose also significantly increased the apoptotic cell population compared with normal glucose and mannitol groups. However, EGCG combined with high glucose greatly decreased the apoptotic cell number compared with high glucose treatment alone. Furthermore, high glucose treatment was demonstrated to significantly increase glucose‑regulated protein 78 (GRP78), phosphorylated‑ PKR‑like ER kinase (p‑PERK) and caspase‑12 protein expression levels, which is representative of endoplasmic reticulum (ER) stress, compared with the normal glucose and mannitol groups. However, EGCG treatment significantly attenuated GRP78, p‑PERK and caspase‑12 protein expression induced by high glucose. These findings suggested that EGCG serves a protective role in glucose‑induced podocyte apoptosis via suppressing ER stress, and may provide a novel therapeutic strategy to ameliorate the process of DN.