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Hyperoside Protects Human Umbilical Vein Endothelial Cells Against Anticardiolipin Antibody-Induced Injury by Activating Autophagy

Anticardiolipin antibody (aCL), an important characterization of antiphospholipid syndrome, shows an intense association with vascular endothelial injury. Hyperoside is a flavonoid extracted from medicinal plants traditionally used in Chinese medicines, displaying anti-inflammatory, anti-cancer, and...

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Autores principales: Wei, Aiwu, Xiao, Huidongzi, Xu, Guangli, Yu, Xile, Guo, Jingjing, Jing, Zhuqing, Shi, Shaoqi, Song, Yanli
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7253676/
https://www.ncbi.nlm.nih.gov/pubmed/32508661
http://dx.doi.org/10.3389/fphar.2020.00762
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author Wei, Aiwu
Xiao, Huidongzi
Xu, Guangli
Yu, Xile
Guo, Jingjing
Jing, Zhuqing
Shi, Shaoqi
Song, Yanli
author_facet Wei, Aiwu
Xiao, Huidongzi
Xu, Guangli
Yu, Xile
Guo, Jingjing
Jing, Zhuqing
Shi, Shaoqi
Song, Yanli
author_sort Wei, Aiwu
collection PubMed
description Anticardiolipin antibody (aCL), an important characterization of antiphospholipid syndrome, shows an intense association with vascular endothelial injury. Hyperoside is a flavonoid extracted from medicinal plants traditionally used in Chinese medicines, displaying anti-inflammatory, anti-cancer, and anti-oxidative properties in various diseases. Recent studies have shifted the focus on the protective effects of hyperoside on vascular endothelial injury. However, little is known about the mechanisms involved. In the present study, we investigated the effect of hyperoside on aCL-induced injury of human umbilical vein endothelial cells (HUVECs) in vitro. Our data illustrated that aCL induced HUVEC injury via inhibiting autophagy. Hyperoside reduced aCL-induced secretion of proinflammatory cytokines IL-1β and IL-8 and endothelial adhesion cytokines TF, ICAM1, and VCAM1 in HUVECs. Additionally, hyperoside activated autophagy and suppressed the mTOR/S6K and TLR4/Myd88/NF-κB signaling transduction pathways in aCL-induced HUVECs. To the best of our knowledge, this is the first study to investigate the effect of hyperoside on aCL-induced injury, as well as offer insights into the involved mechanisms, which is of great significance for the treatment of antiphospholipid syndrome.
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spelling pubmed-72536762020-06-05 Hyperoside Protects Human Umbilical Vein Endothelial Cells Against Anticardiolipin Antibody-Induced Injury by Activating Autophagy Wei, Aiwu Xiao, Huidongzi Xu, Guangli Yu, Xile Guo, Jingjing Jing, Zhuqing Shi, Shaoqi Song, Yanli Front Pharmacol Pharmacology Anticardiolipin antibody (aCL), an important characterization of antiphospholipid syndrome, shows an intense association with vascular endothelial injury. Hyperoside is a flavonoid extracted from medicinal plants traditionally used in Chinese medicines, displaying anti-inflammatory, anti-cancer, and anti-oxidative properties in various diseases. Recent studies have shifted the focus on the protective effects of hyperoside on vascular endothelial injury. However, little is known about the mechanisms involved. In the present study, we investigated the effect of hyperoside on aCL-induced injury of human umbilical vein endothelial cells (HUVECs) in vitro. Our data illustrated that aCL induced HUVEC injury via inhibiting autophagy. Hyperoside reduced aCL-induced secretion of proinflammatory cytokines IL-1β and IL-8 and endothelial adhesion cytokines TF, ICAM1, and VCAM1 in HUVECs. Additionally, hyperoside activated autophagy and suppressed the mTOR/S6K and TLR4/Myd88/NF-κB signaling transduction pathways in aCL-induced HUVECs. To the best of our knowledge, this is the first study to investigate the effect of hyperoside on aCL-induced injury, as well as offer insights into the involved mechanisms, which is of great significance for the treatment of antiphospholipid syndrome. Frontiers Media S.A. 2020-05-21 /pmc/articles/PMC7253676/ /pubmed/32508661 http://dx.doi.org/10.3389/fphar.2020.00762 Text en Copyright © 2020 Wei, Xiao, Xu, Yu, Guo, Jing, Shi and Song http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Pharmacology
Wei, Aiwu
Xiao, Huidongzi
Xu, Guangli
Yu, Xile
Guo, Jingjing
Jing, Zhuqing
Shi, Shaoqi
Song, Yanli
Hyperoside Protects Human Umbilical Vein Endothelial Cells Against Anticardiolipin Antibody-Induced Injury by Activating Autophagy
title Hyperoside Protects Human Umbilical Vein Endothelial Cells Against Anticardiolipin Antibody-Induced Injury by Activating Autophagy
title_full Hyperoside Protects Human Umbilical Vein Endothelial Cells Against Anticardiolipin Antibody-Induced Injury by Activating Autophagy
title_fullStr Hyperoside Protects Human Umbilical Vein Endothelial Cells Against Anticardiolipin Antibody-Induced Injury by Activating Autophagy
title_full_unstemmed Hyperoside Protects Human Umbilical Vein Endothelial Cells Against Anticardiolipin Antibody-Induced Injury by Activating Autophagy
title_short Hyperoside Protects Human Umbilical Vein Endothelial Cells Against Anticardiolipin Antibody-Induced Injury by Activating Autophagy
title_sort hyperoside protects human umbilical vein endothelial cells against anticardiolipin antibody-induced injury by activating autophagy
topic Pharmacology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7253676/
https://www.ncbi.nlm.nih.gov/pubmed/32508661
http://dx.doi.org/10.3389/fphar.2020.00762
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