Epigallocatechin-3-gallate inhibits H2O2-induced apoptosis in Mouse Vascular Smooth Muscle Cells via 67kD Laminin Receptor

Abstract Epigallocatechin-3-gallate (EGCG) is one of the major polyphenolic compounds present in green tea extracts and has been used as a potential drug for the treatment of numerous diseases. The present study aimed to elucidate the role and mechanism of EGCG in protecting against H2O2-induced apo...

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Autores principales:	Xue Yan, Yanfei Li, Han Yu, Wei Wang, Chunyan Wu, Yang Yang, Yongjia Hu, Xiujuan Shi, Jue Li
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/0f869f61ed504f27b8f4fd7d3fcf02d2
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spelling	oai:doaj.org-article:0f869f61ed504f27b8f4fd7d3fcf02d22021-12-02T12:32:27ZEpigallocatechin-3-gallate inhibits H2O2-induced apoptosis in Mouse Vascular Smooth Muscle Cells via 67kD Laminin Receptor10.1038/s41598-017-08301-62045-2322https://doaj.org/article/0f869f61ed504f27b8f4fd7d3fcf02d22017-08-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-08301-6https://doaj.org/toc/2045-2322Abstract Epigallocatechin-3-gallate (EGCG) is one of the major polyphenolic compounds present in green tea extracts and has been used as a potential drug for the treatment of numerous diseases. The present study aimed to elucidate the role and mechanism of EGCG in protecting against H2O2-induced apoptosis in mouse vascular smooth muscle cells (VSMCs). VSMCs were pretreated with various concentrations of EGCG for 2 hours prior to treatment with H2O2. Treatment with H2O2 significantly decreased the cell viability and induced apoptosis of VSMCs, which were attenuated by pretreatment with EGCG. In particular, EGCG pretreatment significantly inhibited the H2O2-induced upregulation of cleaved forms of caspase-3, caspase-8, and caspase-9, Bax, CathepsinD, and downregulation of Bcl-2. Moreover, the antioxidation effect of EGCG on VSMCs was determined to be associated with the 67kD laminin receptor (67LR). Our results demonstrated that EGCG improved cell viability and protected VSMCs against oxidative stress through both extrinsic and intrinsic pathways, while 67LR is likely to be an active and key receptor of EGCG. These findings provide a novel molecular mechanism of EGCG in inhibiting H2O2-induced apoptosis in VSMCs, as well as its function in preventing the development of atherosclerosis.Xue YanYanfei LiHan YuWei WangChunyan WuYang YangYongjia HuXiujuan ShiJue LiNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-10 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Xue Yan Yanfei Li Han Yu Wei Wang Chunyan Wu Yang Yang Yongjia Hu Xiujuan Shi Jue Li Epigallocatechin-3-gallate inhibits H2O2-induced apoptosis in Mouse Vascular Smooth Muscle Cells via 67kD Laminin Receptor
description	Abstract Epigallocatechin-3-gallate (EGCG) is one of the major polyphenolic compounds present in green tea extracts and has been used as a potential drug for the treatment of numerous diseases. The present study aimed to elucidate the role and mechanism of EGCG in protecting against H2O2-induced apoptosis in mouse vascular smooth muscle cells (VSMCs). VSMCs were pretreated with various concentrations of EGCG for 2 hours prior to treatment with H2O2. Treatment with H2O2 significantly decreased the cell viability and induced apoptosis of VSMCs, which were attenuated by pretreatment with EGCG. In particular, EGCG pretreatment significantly inhibited the H2O2-induced upregulation of cleaved forms of caspase-3, caspase-8, and caspase-9, Bax, CathepsinD, and downregulation of Bcl-2. Moreover, the antioxidation effect of EGCG on VSMCs was determined to be associated with the 67kD laminin receptor (67LR). Our results demonstrated that EGCG improved cell viability and protected VSMCs against oxidative stress through both extrinsic and intrinsic pathways, while 67LR is likely to be an active and key receptor of EGCG. These findings provide a novel molecular mechanism of EGCG in inhibiting H2O2-induced apoptosis in VSMCs, as well as its function in preventing the development of atherosclerosis.
format	article
author	Xue Yan Yanfei Li Han Yu Wei Wang Chunyan Wu Yang Yang Yongjia Hu Xiujuan Shi Jue Li
author_facet	Xue Yan Yanfei Li Han Yu Wei Wang Chunyan Wu Yang Yang Yongjia Hu Xiujuan Shi Jue Li
author_sort	Xue Yan
title	Epigallocatechin-3-gallate inhibits H2O2-induced apoptosis in Mouse Vascular Smooth Muscle Cells via 67kD Laminin Receptor
title_short	Epigallocatechin-3-gallate inhibits H2O2-induced apoptosis in Mouse Vascular Smooth Muscle Cells via 67kD Laminin Receptor
title_full	Epigallocatechin-3-gallate inhibits H2O2-induced apoptosis in Mouse Vascular Smooth Muscle Cells via 67kD Laminin Receptor
title_fullStr	Epigallocatechin-3-gallate inhibits H2O2-induced apoptosis in Mouse Vascular Smooth Muscle Cells via 67kD Laminin Receptor
title_full_unstemmed	Epigallocatechin-3-gallate inhibits H2O2-induced apoptosis in Mouse Vascular Smooth Muscle Cells via 67kD Laminin Receptor
title_sort	epigallocatechin-3-gallate inhibits h2o2-induced apoptosis in mouse vascular smooth muscle cells via 67kd laminin receptor
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/0f869f61ed504f27b8f4fd7d3fcf02d2
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Epigallocatechin-3-gallate inhibits H2O2-induced apoptosis in Mouse Vascular Smooth Muscle Cells via 67kD Laminin Receptor

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