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Epigallocatechin-3-gallate inhibits H(2)O(2)-induced apoptosis in Mouse Vascular Smooth Muscle Cells via 67kD Laminin Receptor

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 H(2)O(2)-induced apoptosi...

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Autores principales: Yan, Xue, Li, Yanfei, Yu, Han, Wang, Wei, Wu, Chunyan, Yang, Yang, Hu, Yongjia, Shi, Xiujuan, Li, Jue
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5552808/
https://www.ncbi.nlm.nih.gov/pubmed/28798484
http://dx.doi.org/10.1038/s41598-017-08301-6
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author Yan, Xue
Li, Yanfei
Yu, Han
Wang, Wei
Wu, Chunyan
Yang, Yang
Hu, Yongjia
Shi, Xiujuan
Li, Jue
author_facet Yan, Xue
Li, Yanfei
Yu, Han
Wang, Wei
Wu, Chunyan
Yang, Yang
Hu, Yongjia
Shi, Xiujuan
Li, Jue
author_sort Yan, Xue
collection PubMed
description 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 H(2)O(2)-induced apoptosis in mouse vascular smooth muscle cells (VSMCs). VSMCs were pretreated with various concentrations of EGCG for 2 hours prior to treatment with H(2)O(2). Treatment with H(2)O(2) significantly decreased the cell viability and induced apoptosis of VSMCs, which were attenuated by pretreatment with EGCG. In particular, EGCG pretreatment significantly inhibited the H(2)O(2)-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 H(2)O(2)-induced apoptosis in VSMCs, as well as its function in preventing the development of atherosclerosis.
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spelling pubmed-55528082017-08-14 Epigallocatechin-3-gallate inhibits H(2)O(2)-induced apoptosis in Mouse Vascular Smooth Muscle Cells via 67kD Laminin Receptor Yan, Xue Li, Yanfei Yu, Han Wang, Wei Wu, Chunyan Yang, Yang Hu, Yongjia Shi, Xiujuan Li, Jue Sci Rep Article 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 H(2)O(2)-induced apoptosis in mouse vascular smooth muscle cells (VSMCs). VSMCs were pretreated with various concentrations of EGCG for 2 hours prior to treatment with H(2)O(2). Treatment with H(2)O(2) significantly decreased the cell viability and induced apoptosis of VSMCs, which were attenuated by pretreatment with EGCG. In particular, EGCG pretreatment significantly inhibited the H(2)O(2)-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 H(2)O(2)-induced apoptosis in VSMCs, as well as its function in preventing the development of atherosclerosis. Nature Publishing Group UK 2017-08-10 /pmc/articles/PMC5552808/ /pubmed/28798484 http://dx.doi.org/10.1038/s41598-017-08301-6 Text en © The Author(s) 2017 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Article
Yan, Xue
Li, Yanfei
Yu, Han
Wang, Wei
Wu, Chunyan
Yang, Yang
Hu, Yongjia
Shi, Xiujuan
Li, Jue
Epigallocatechin-3-gallate inhibits H(2)O(2)-induced apoptosis in Mouse Vascular Smooth Muscle Cells via 67kD Laminin Receptor
title Epigallocatechin-3-gallate inhibits H(2)O(2)-induced apoptosis in Mouse Vascular Smooth Muscle Cells via 67kD Laminin Receptor
title_full Epigallocatechin-3-gallate inhibits H(2)O(2)-induced apoptosis in Mouse Vascular Smooth Muscle Cells via 67kD Laminin Receptor
title_fullStr Epigallocatechin-3-gallate inhibits H(2)O(2)-induced apoptosis in Mouse Vascular Smooth Muscle Cells via 67kD Laminin Receptor
title_full_unstemmed Epigallocatechin-3-gallate inhibits H(2)O(2)-induced apoptosis in Mouse Vascular Smooth Muscle Cells via 67kD Laminin Receptor
title_short Epigallocatechin-3-gallate inhibits H(2)O(2)-induced apoptosis in Mouse Vascular Smooth Muscle Cells via 67kD Laminin Receptor
title_sort epigallocatechin-3-gallate inhibits h(2)o(2)-induced apoptosis in mouse vascular smooth muscle cells via 67kd laminin receptor
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5552808/
https://www.ncbi.nlm.nih.gov/pubmed/28798484
http://dx.doi.org/10.1038/s41598-017-08301-6
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