Upregulation and stabilization of senescence marker protein-30 by epigallocatechin gallate against -butyl hydroperoxide-induced liver injury and .

Senescence marker protein-30 (SMP30), a novel ageing marker, suppresses oxidative stress in the liver. However, studies on phytochemical-mediated regulation of SMP30 expression are lacking. Here, we showed that epigallocatechin gallate (EGCg), a polyphenol abundant in green tea, positively regulates SMP30 expression in the rat hepatoma-derived Fao cells. EGCg maintained SMP30 expression even in the presence of cycloheximide, a protein synthesis inhibitor. Furthermore, treatment of cells with -butyl hydroperoxide (-BHP), an oxidative promoter, decreased SMP30 expression and ERK1/2 phosphorylation, while EGCg treatment inhibited these effects. Male mice (7-week-old) were divided into 4 groups-Control (saline), -BHP (1.5 mmol/kg -BHP), EGCg + -BHP (30 mg/kg/day of EGCg and 1.5 mmol/kg -BHP), and EGCg (30 mg/kg/day). After oral EGCg administration for 6 consecutive days, EGCg + -BHP group mice were administered -BHP. The -BHP-administered mice showed decreased SMP30 expression in the liver and increased aspartate aminotransferase and alanine transaminase (hepatic injury marker enzymes) activities; however, EGCg treatment attenuated these changes. Thus, EGCg-induced SMP30 upregulation may alleviate -BHP-induced liver injury. The findings of this study offer new perspectives of the anti-ageing properties of EGCg.