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

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...

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Autores principales: Inoue, Hirofumi, Arakawa, Kohta, Tanaka, Miori, Katsumata-Tsuboi, Rie, Takahashi, Nobuyuki, Uehara, Mariko
Formato: Online Artículo Texto
Lenguaje:English
Publicado: the Society for Free Radical Research Japan 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7844653/
https://www.ncbi.nlm.nih.gov/pubmed/33536712
http://dx.doi.org/10.3164/jcbn.20-119
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author Inoue, Hirofumi
Arakawa, Kohta
Tanaka, Miori
Katsumata-Tsuboi, Rie
Takahashi, Nobuyuki
Uehara, Mariko
author_facet Inoue, Hirofumi
Arakawa, Kohta
Tanaka, Miori
Katsumata-Tsuboi, Rie
Takahashi, Nobuyuki
Uehara, Mariko
author_sort Inoue, Hirofumi
collection PubMed
description 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.
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spelling pubmed-78446532021-02-02 Upregulation and stabilization of senescence marker protein-30 by epigallocatechin gallate against tert-butyl hydroperoxide-induced liver injury in vitro and in vivo Inoue, Hirofumi Arakawa, Kohta Tanaka, Miori Katsumata-Tsuboi, Rie Takahashi, Nobuyuki Uehara, Mariko J Clin Biochem Nutr Original Article 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. the Society for Free Radical Research Japan 2021-01 2020-11-14 /pmc/articles/PMC7844653/ /pubmed/33536712 http://dx.doi.org/10.3164/jcbn.20-119 Text en Copyright © 2021 JCBN http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives License (http://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle Original Article
Inoue, Hirofumi
Arakawa, Kohta
Tanaka, Miori
Katsumata-Tsuboi, Rie
Takahashi, Nobuyuki
Uehara, Mariko
Upregulation and stabilization of senescence marker protein-30 by epigallocatechin gallate against tert-butyl hydroperoxide-induced liver injury in vitro and in vivo
title Upregulation and stabilization of senescence marker protein-30 by epigallocatechin gallate against tert-butyl hydroperoxide-induced liver injury in vitro and in vivo
title_full Upregulation and stabilization of senescence marker protein-30 by epigallocatechin gallate against tert-butyl hydroperoxide-induced liver injury in vitro and in vivo
title_fullStr Upregulation and stabilization of senescence marker protein-30 by epigallocatechin gallate against tert-butyl hydroperoxide-induced liver injury in vitro and in vivo
title_full_unstemmed Upregulation and stabilization of senescence marker protein-30 by epigallocatechin gallate against tert-butyl hydroperoxide-induced liver injury in vitro and in vivo
title_short Upregulation and stabilization of senescence marker protein-30 by epigallocatechin gallate against tert-butyl hydroperoxide-induced liver injury in vitro and in vivo
title_sort upregulation and stabilization of senescence marker protein-30 by epigallocatechin gallate against tert-butyl hydroperoxide-induced liver injury in vitro and in vivo
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7844653/
https://www.ncbi.nlm.nih.gov/pubmed/33536712
http://dx.doi.org/10.3164/jcbn.20-119
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