Upregulation and stabilization of senescence marker protein-30 by epigallocatechin gallate against <i>tert</i>-butyl hydroperoxide-induced liver injury <i>in vitro</i> and <i>in vivo</i>

DOI Web Site 被引用文献2件 参考文献37件 オープンアクセス
  • Inoue Hirofumi
    Department of Nutritional Science and Food Safety, Faculty of Applied Bioscience, Tokyo University of Agriculture
  • Arakawa Kohta
    Department of Nutritional Science and Food Safety, Faculty of Applied Bioscience, Tokyo University of Agriculture
  • Tanaka Miori
    Department of Nutritional Science and Food Safety, Faculty of Applied Bioscience, Tokyo University of Agriculture
  • Katsumata-Tsuboi Rie
    Department of Nutritional Science and Food Safety, Faculty of Applied Bioscience, Tokyo University of Agriculture
  • Takahashi Nobuyuki
    Department of Nutritional Science and Food Safety, Faculty of Applied Bioscience, Tokyo University of Agriculture
  • Uehara Mariko
    Department of Nutritional Science and Food Safety, Faculty of Applied Bioscience, Tokyo University of Agriculture

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<p>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 tert-butyl hydroperoxide (tert-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), tert-BHP (1.5 mmol/kg tert-BHP), EGCg + tert-BHP (30 mg/kg/day of EGCg and 1.5 mmol/kg tert-BHP), and EGCg (30 mg/kg/day). After oral EGCg administration for 6 consecutive days, EGCg + tert-BHP group mice were administered tert-BHP. The tert-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 tert-BHP-induced liver injury. The findings of this study offer new perspectives of the anti-ageing properties of EGCg.</p>

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