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

Hyperoside Protects Human Umbilical Vein Endothelial Cells Against Anticardiolipin Antibody-Induced Injury by Activating Autophagy
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金丝桃苷通过激活自噬保护人脐静脉内皮细胞免受抗心磷脂抗体诱导的损伤

DOI:
10.3389/fphar.2020.00762
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发表时间:
2020-05-21
影响因子:
5.6
通讯作者:
Song, Yanli
Song, Yanli
中科院分区:
医学2区
文献类型:
--
作者:
Wei, Aiwu;Xiao, Huidongzi;Song, Yanli

文献摘要

被引文献

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抗心磷脂抗体(aCL)是抗磷脂综合征的重要特征,与血管内皮损伤密切相关。金丝桃苷是从传统中药中使用的药用植物中提取的黄酮类化合物,在各种疾病中显示出抗炎,抗癌和抗氧化特性。金丝桃苷对血管内皮损伤的保护作用是近年来研究的热点。然而,人们对所涉及的机制知之甚少。本研究观察了金丝桃苷对ACL诱导的体外培养人脐静脉内皮细胞(HUVECs)损伤的影响。我们的数据表明,ACL通过抑制自噬诱导HUVEC损伤。金丝桃苷减少aCL诱导的促炎细胞因子IL-1β和IL-8以及内皮粘附细胞因子TF、ICAM 1和VCAM 1在HUVEC中的分泌。此外,金丝桃苷还能激活aCL诱导的HUVECs自噬,抑制mTOR/S6 K和TLR 4/Myd 88/NF-κB信号转导通路。据我们所知,这是第一个研究金丝桃苷对aCL诱导的损伤的影响,并提供了有关机制的见解,这对于抗磷脂综合征的治疗具有重要意义。
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.