Epigallocatechin-3-gallate protects cardiomyocytes from hypoxia-reoxygenation damage via raising autophagy related 4C expression

Myocardial ischemia/reperfusion (I/R) injury is a serious issue during the therapy of myocardial infarction. Herein, we explored the beneficial influence of Epigallocatechin-3-gallate (EGCG) on hypoxia/reoxygenation (H/R)-stimulated cardiomyocyte H9c2 cells damage, along with possible internal molec...

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Autores principales:	Ping Liu, Jin Huang, Wanzhen Mei, Xingfang Zeng, Cheng Wang, Chuan Wen, Jing Xu
Formato:	article
Lenguaje:	EN
Publicado:	Taylor & Francis Group 2021
Materias:	myocardial ischemia/reperfusion cardiomyocyte hypoxia/reoxygenation epigallocatechin-3-gallate h9c2 cells reactive oxygen species autophagy related 4c Biotechnology TP248.13-248.65
Acceso en línea:	https://doaj.org/article/b45933c4a10d40559990a7a736ea310a
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spelling	oai:doaj.org-article:b45933c4a10d40559990a7a736ea310a2021-11-04T15:51:54ZEpigallocatechin-3-gallate protects cardiomyocytes from hypoxia-reoxygenation damage via raising autophagy related 4C expression2165-59792165-598710.1080/21655979.2021.1996018https://doaj.org/article/b45933c4a10d40559990a7a736ea310a2021-10-01T00:00:00Zhttp://dx.doi.org/10.1080/21655979.2021.1996018https://doaj.org/toc/2165-5979https://doaj.org/toc/2165-5987Myocardial ischemia/reperfusion (I/R) injury is a serious issue during the therapy of myocardial infarction. Herein, we explored the beneficial influence of Epigallocatechin-3-gallate (EGCG) on hypoxia/reoxygenation (H/R)-stimulated cardiomyocyte H9c2 cells damage, along with possible internal molecular mechanism related autophagy related 4C (ATG4C). H9c2 cells were subjected to H/R stimulation and/or EGCG treatment. ATG4C mRNA expression was measured via q-PCR assay. ATG4C overexpression plasmid (OE-ATG4C) was transfected to arise ATG4C level. Cell viability, apoptosis, reactive oxygen species (ROS) production, ATP level were tested via CCK-8 assay, Annexin V-FITC/PI staining, DCFH-DA staining and ATP Assay Kit, respectively. Western blotting was performed to test Cleaved-caspase 3, Cleaved-caspase 9, cytochrome C and LC3B protein levels. H/R stimulation resulted in H9c2 cell viability loss, promoted cell apoptosis and ROS overproduction, as well as lowered ATP level in cells. EGCG treatment alleviated H/R-resulted H9c2 cell viability loss, cell apoptosis, ROS overproduction and reduction of ATP level. Moreover, H/R stimulation reduced the ATG4C expression in H9c2 cells, while EGCG raised the ATG4C expression. Overexpression of ATG4C strengthened the beneficial influence of EGCG on H/R-stimulated H9c2 cell viability, apoptosis and ROS production. Besides, ATG4C overexpression weakened the H/R-stimulated H9c2 cell autophagy via reducing LC3B II/I expression. EGCG exerted beneficial influence on H/R-stimulated cardiomyocytes, which protected cardiomyocytes from H/R-stimulated viability loss, apoptosis and ROS overproduction via enhancing ATG4C expression.Ping LiuJin HuangWanzhen MeiXingfang ZengCheng WangChuan WenJing XuTaylor & Francis Grouparticlemyocardial ischemia/reperfusioncardiomyocyte hypoxia/reoxygenationepigallocatechin-3-gallateh9c2 cellsreactive oxygen speciesautophagy related 4cBiotechnologyTP248.13-248.65ENBioengineered, Vol 0, Iss 0 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	myocardial ischemia/reperfusion cardiomyocyte hypoxia/reoxygenation epigallocatechin-3-gallate h9c2 cells reactive oxygen species autophagy related 4c Biotechnology TP248.13-248.65
spellingShingle	myocardial ischemia/reperfusion cardiomyocyte hypoxia/reoxygenation epigallocatechin-3-gallate h9c2 cells reactive oxygen species autophagy related 4c Biotechnology TP248.13-248.65 Ping Liu Jin Huang Wanzhen Mei Xingfang Zeng Cheng Wang Chuan Wen Jing Xu Epigallocatechin-3-gallate protects cardiomyocytes from hypoxia-reoxygenation damage via raising autophagy related 4C expression
description	Myocardial ischemia/reperfusion (I/R) injury is a serious issue during the therapy of myocardial infarction. Herein, we explored the beneficial influence of Epigallocatechin-3-gallate (EGCG) on hypoxia/reoxygenation (H/R)-stimulated cardiomyocyte H9c2 cells damage, along with possible internal molecular mechanism related autophagy related 4C (ATG4C). H9c2 cells were subjected to H/R stimulation and/or EGCG treatment. ATG4C mRNA expression was measured via q-PCR assay. ATG4C overexpression plasmid (OE-ATG4C) was transfected to arise ATG4C level. Cell viability, apoptosis, reactive oxygen species (ROS) production, ATP level were tested via CCK-8 assay, Annexin V-FITC/PI staining, DCFH-DA staining and ATP Assay Kit, respectively. Western blotting was performed to test Cleaved-caspase 3, Cleaved-caspase 9, cytochrome C and LC3B protein levels. H/R stimulation resulted in H9c2 cell viability loss, promoted cell apoptosis and ROS overproduction, as well as lowered ATP level in cells. EGCG treatment alleviated H/R-resulted H9c2 cell viability loss, cell apoptosis, ROS overproduction and reduction of ATP level. Moreover, H/R stimulation reduced the ATG4C expression in H9c2 cells, while EGCG raised the ATG4C expression. Overexpression of ATG4C strengthened the beneficial influence of EGCG on H/R-stimulated H9c2 cell viability, apoptosis and ROS production. Besides, ATG4C overexpression weakened the H/R-stimulated H9c2 cell autophagy via reducing LC3B II/I expression. EGCG exerted beneficial influence on H/R-stimulated cardiomyocytes, which protected cardiomyocytes from H/R-stimulated viability loss, apoptosis and ROS overproduction via enhancing ATG4C expression.
format	article
author	Ping Liu Jin Huang Wanzhen Mei Xingfang Zeng Cheng Wang Chuan Wen Jing Xu
author_facet	Ping Liu Jin Huang Wanzhen Mei Xingfang Zeng Cheng Wang Chuan Wen Jing Xu
author_sort	Ping Liu
title	Epigallocatechin-3-gallate protects cardiomyocytes from hypoxia-reoxygenation damage via raising autophagy related 4C expression
title_short	Epigallocatechin-3-gallate protects cardiomyocytes from hypoxia-reoxygenation damage via raising autophagy related 4C expression
title_full	Epigallocatechin-3-gallate protects cardiomyocytes from hypoxia-reoxygenation damage via raising autophagy related 4C expression
title_fullStr	Epigallocatechin-3-gallate protects cardiomyocytes from hypoxia-reoxygenation damage via raising autophagy related 4C expression
title_full_unstemmed	Epigallocatechin-3-gallate protects cardiomyocytes from hypoxia-reoxygenation damage via raising autophagy related 4C expression
title_sort	epigallocatechin-3-gallate protects cardiomyocytes from hypoxia-reoxygenation damage via raising autophagy related 4c expression
publisher	Taylor & Francis Group
publishDate	2021
url	https://doaj.org/article/b45933c4a10d40559990a7a736ea310a
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Epigallocatechin-3-gallate protects cardiomyocytes from hypoxia-reoxygenation damage via raising autophagy related 4C expression

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