Inoue Hirofumi, Arakawa Kohta, Tanaka Miori, Katsumata-Tsuboi Rie, Takahashi Nobuyuki, Uehara Mariko
Department of Nutritional Science and Food Safety, Faculty of Applied Bioscience, Tokyo University of Agriculture, 1-1-1 Sakuragaoka, Setagaya-ku, Tokyo 156-8502, Japan.
J Clin Biochem Nutr. 2021 Jan;68(1):51-57. doi: 10.3164/jcbn.20-119. Epub 2020 Nov 14.
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.
衰老标志物蛋白-30（SMP30）是一种新型衰老标志物，可抑制肝脏中的氧化应激。然而，关于植物化学物质介导的SMP30表达调控的研究尚属空白。在此，我们发现表没食子儿茶素没食子酸酯（EGCg），一种绿茶中富含的多酚，可正向调控大鼠肝癌衍生的Fao细胞中SMP30的表达。即使在存在蛋白质合成抑制剂环己酰亚胺的情况下，EGCg仍能维持SMP30的表达。此外，用氧化促进剂叔丁基过氧化氢（t-BHP）处理细胞会降低SMP30的表达和ERK1/2磷酸化，而EGCg处理可抑制这些作用。将雄性小鼠（7周龄）分为4组——对照组（生理盐水）、t-BHP组（1.5 mmol/kg t-BHP）、EGCg + t-BHP组（30 mg/kg/天的EGCg和1.5 mmol/kg t-BHP）和EGCg组（30 mg/kg/天）。连续口服EGCg 6天后，给EGCg + t-BHP组小鼠注射t-BHP。注射t-BHP的小鼠肝脏中SMP30表达降低，天冬氨酸转氨酶和丙氨酸转氨酶（肝损伤标志物酶）活性升高；然而，EGCg处理减轻了这些变化。因此，EGCg诱导的SMP30上调可能减轻t-BHP诱导的肝损伤。本研究结果为EGCg的抗衰老特性提供了新的视角。
