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Epigallocatechin-3-gallate attenuates neointimal hyperplasia in a rat model of carotid artery injury by inhibition of high mobility group box 1 expression
Epigallocatechin-3-gallate (EGCG) is a kind of polyphenol compound, called catechin, and is extracted from green tea. EGCG has a wide range of biological activities. The present study aimed to evaluate the effect of EGCG on neointimal hyperplasia in a rat model of carotid artery balloon injury and t...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5609174/ https://www.ncbi.nlm.nih.gov/pubmed/28962112 http://dx.doi.org/10.3892/etm.2017.4774 |
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author | Yang, Bin Gao, Peng Wu, Xuejun Yu, Jixiang Li, Yu Meng, Ranran Li, Yubin Yan, Jingqiang Jin, Xing |
author_facet | Yang, Bin Gao, Peng Wu, Xuejun Yu, Jixiang Li, Yu Meng, Ranran Li, Yubin Yan, Jingqiang Jin, Xing |
author_sort | Yang, Bin |
collection | PubMed |
description | Epigallocatechin-3-gallate (EGCG) is a kind of polyphenol compound, called catechin, and is extracted from green tea. EGCG has a wide range of biological activities. The present study aimed to evaluate the effect of EGCG on neointimal hyperplasia in a rat model of carotid artery balloon injury and to explore the molecular mechanisms involved. Various experiments were performed to assess the effects of EGCG on thickening of neointima, expression levels of high mobility group box 1 protein (HMGB1) and receptor of advanced glycation end products (RAGE), the inflammatory response, oxidative stress and activation of nuclear factor (NF)-κB. Results demonstrated that EGCG decreased the intimal area and the ratio of intimal area/medial area compared with the balloon injury group. The expression levels of HMGB1 and RAGE induced by balloon injury were markedly inhibited by EGCG treatment. Furthermore, the inflammatory response and oxidative stress damage, which have close correlations with HMGB1, were restrained by EGCG. Finally, EGCG treatment markedly inhibited NF-κB activation. The present data provided evidence that EGCG attenuates neointimal hyperplasia in a model of carotid artery balloon injury, which indicated that EGCG may serve as a potential drug for restenosis in clinics. |
format | Online Article Text |
id | pubmed-5609174 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-56091742017-09-28 Epigallocatechin-3-gallate attenuates neointimal hyperplasia in a rat model of carotid artery injury by inhibition of high mobility group box 1 expression Yang, Bin Gao, Peng Wu, Xuejun Yu, Jixiang Li, Yu Meng, Ranran Li, Yubin Yan, Jingqiang Jin, Xing Exp Ther Med Articles Epigallocatechin-3-gallate (EGCG) is a kind of polyphenol compound, called catechin, and is extracted from green tea. EGCG has a wide range of biological activities. The present study aimed to evaluate the effect of EGCG on neointimal hyperplasia in a rat model of carotid artery balloon injury and to explore the molecular mechanisms involved. Various experiments were performed to assess the effects of EGCG on thickening of neointima, expression levels of high mobility group box 1 protein (HMGB1) and receptor of advanced glycation end products (RAGE), the inflammatory response, oxidative stress and activation of nuclear factor (NF)-κB. Results demonstrated that EGCG decreased the intimal area and the ratio of intimal area/medial area compared with the balloon injury group. The expression levels of HMGB1 and RAGE induced by balloon injury were markedly inhibited by EGCG treatment. Furthermore, the inflammatory response and oxidative stress damage, which have close correlations with HMGB1, were restrained by EGCG. Finally, EGCG treatment markedly inhibited NF-κB activation. The present data provided evidence that EGCG attenuates neointimal hyperplasia in a model of carotid artery balloon injury, which indicated that EGCG may serve as a potential drug for restenosis in clinics. D.A. Spandidos 2017-09 2017-07-11 /pmc/articles/PMC5609174/ /pubmed/28962112 http://dx.doi.org/10.3892/etm.2017.4774 Text en Copyright: © Yang et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Articles Yang, Bin Gao, Peng Wu, Xuejun Yu, Jixiang Li, Yu Meng, Ranran Li, Yubin Yan, Jingqiang Jin, Xing Epigallocatechin-3-gallate attenuates neointimal hyperplasia in a rat model of carotid artery injury by inhibition of high mobility group box 1 expression |
title | Epigallocatechin-3-gallate attenuates neointimal hyperplasia in a rat model of carotid artery injury by inhibition of high mobility group box 1 expression |
title_full | Epigallocatechin-3-gallate attenuates neointimal hyperplasia in a rat model of carotid artery injury by inhibition of high mobility group box 1 expression |
title_fullStr | Epigallocatechin-3-gallate attenuates neointimal hyperplasia in a rat model of carotid artery injury by inhibition of high mobility group box 1 expression |
title_full_unstemmed | Epigallocatechin-3-gallate attenuates neointimal hyperplasia in a rat model of carotid artery injury by inhibition of high mobility group box 1 expression |
title_short | Epigallocatechin-3-gallate attenuates neointimal hyperplasia in a rat model of carotid artery injury by inhibition of high mobility group box 1 expression |
title_sort | epigallocatechin-3-gallate attenuates neointimal hyperplasia in a rat model of carotid artery injury by inhibition of high mobility group box 1 expression |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5609174/ https://www.ncbi.nlm.nih.gov/pubmed/28962112 http://dx.doi.org/10.3892/etm.2017.4774 |
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