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Protective effects of quercetin and taraxasterol against H(2)O(2)-induced human umbilical vein endothelial cell injury in vitro

Due to the association between inflammation and endothelial dysfunction in atherosclerosis, the blockage of the inflammatory process that occurs on the endothelial cells may be a useful way of preventing atherosclerosis. In the present study, human umbilical vein endothelial cells (HUVECs) were used...

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Autores principales: YANG, DONGWEI, LIU, XINYE, LIU, MIN, CHI, HAO, LIU, JIRONG, HAN, HUAMIN
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4578013/
https://www.ncbi.nlm.nih.gov/pubmed/26622474
http://dx.doi.org/10.3892/etm.2015.2713
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author YANG, DONGWEI
LIU, XINYE
LIU, MIN
CHI, HAO
LIU, JIRONG
HAN, HUAMIN
author_facet YANG, DONGWEI
LIU, XINYE
LIU, MIN
CHI, HAO
LIU, JIRONG
HAN, HUAMIN
author_sort YANG, DONGWEI
collection PubMed
description Due to the association between inflammation and endothelial dysfunction in atherosclerosis, the blockage of the inflammatory process that occurs on the endothelial cells may be a useful way of preventing atherosclerosis. In the present study, human umbilical vein endothelial cells (HUVECs) were used to investigate the protective effects of quercetin and taraxasterol against H(2)O(2)-induced oxidative damage and inflammation. HUVECs were pretreated with quercetin or taraxasterol at concentrations ranging between 0 and 210 µM for 12 h, prior to being administered different concentrations of H(2)O(2) for 4 h. Cell viability and levels of apoptosis were assessed through cell counting kit-8 (CCK-8) and terminal deoxynucleotidyl transferase dUTP nick end labeling assays, respectively, to determine the injury to the HUVECs. The viability loss in the H(2)O(2)-induced HUVECs was markedly restored in a concentration-dependent manner by pretreatment with quercetin or taraxasterol. This effect was accompanied by significantly decreased expression of vascular cell adhesion molecule 1 (VCAM-1) and cluster of differentiation (CD)80 for taraxasterol and that of CD80 for quercetin. In conclusion, the present study showed the protective effects of quercetin and taraxasterol against cell injury and inflammation in HUVECs and indicated that the effects were mediated via the downregulation of VCAM-1 and CD80 expression. This study has therefore served as a preliminary investigation on the anti-atherosclerotic and cardiovascular protective effects of quercetin and taraxasterol as dietary supplements.
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spelling pubmed-45780132015-11-30 Protective effects of quercetin and taraxasterol against H(2)O(2)-induced human umbilical vein endothelial cell injury in vitro YANG, DONGWEI LIU, XINYE LIU, MIN CHI, HAO LIU, JIRONG HAN, HUAMIN Exp Ther Med Articles Due to the association between inflammation and endothelial dysfunction in atherosclerosis, the blockage of the inflammatory process that occurs on the endothelial cells may be a useful way of preventing atherosclerosis. In the present study, human umbilical vein endothelial cells (HUVECs) were used to investigate the protective effects of quercetin and taraxasterol against H(2)O(2)-induced oxidative damage and inflammation. HUVECs were pretreated with quercetin or taraxasterol at concentrations ranging between 0 and 210 µM for 12 h, prior to being administered different concentrations of H(2)O(2) for 4 h. Cell viability and levels of apoptosis were assessed through cell counting kit-8 (CCK-8) and terminal deoxynucleotidyl transferase dUTP nick end labeling assays, respectively, to determine the injury to the HUVECs. The viability loss in the H(2)O(2)-induced HUVECs was markedly restored in a concentration-dependent manner by pretreatment with quercetin or taraxasterol. This effect was accompanied by significantly decreased expression of vascular cell adhesion molecule 1 (VCAM-1) and cluster of differentiation (CD)80 for taraxasterol and that of CD80 for quercetin. In conclusion, the present study showed the protective effects of quercetin and taraxasterol against cell injury and inflammation in HUVECs and indicated that the effects were mediated via the downregulation of VCAM-1 and CD80 expression. This study has therefore served as a preliminary investigation on the anti-atherosclerotic and cardiovascular protective effects of quercetin and taraxasterol as dietary supplements. D.A. Spandidos 2015-10 2015-08-25 /pmc/articles/PMC4578013/ /pubmed/26622474 http://dx.doi.org/10.3892/etm.2015.2713 Text en Copyright: © Yang et al. This is an open access article distributed under the terms of a Creative Commons Attribution License. http://creativecommons.org/licenses/by/4.0 This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 4.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited.
spellingShingle Articles
YANG, DONGWEI
LIU, XINYE
LIU, MIN
CHI, HAO
LIU, JIRONG
HAN, HUAMIN
Protective effects of quercetin and taraxasterol against H(2)O(2)-induced human umbilical vein endothelial cell injury in vitro
title Protective effects of quercetin and taraxasterol against H(2)O(2)-induced human umbilical vein endothelial cell injury in vitro
title_full Protective effects of quercetin and taraxasterol against H(2)O(2)-induced human umbilical vein endothelial cell injury in vitro
title_fullStr Protective effects of quercetin and taraxasterol against H(2)O(2)-induced human umbilical vein endothelial cell injury in vitro
title_full_unstemmed Protective effects of quercetin and taraxasterol against H(2)O(2)-induced human umbilical vein endothelial cell injury in vitro
title_short Protective effects of quercetin and taraxasterol against H(2)O(2)-induced human umbilical vein endothelial cell injury in vitro
title_sort protective effects of quercetin and taraxasterol against h(2)o(2)-induced human umbilical vein endothelial cell injury in vitro
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4578013/
https://www.ncbi.nlm.nih.gov/pubmed/26622474
http://dx.doi.org/10.3892/etm.2015.2713
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