Protective effects of hyperoside against human umbilical vein endothelial cell damage induced by hydrogen peroxide

Protective effects of hyperoside against human umbilical vein endothelial cell damage induced by hydrogen peroxide
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DOI:
10.1016/j.jep.2011.11.020
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发表时间:
2012-01-31
影响因子:
5.4
通讯作者:
Zhao, Ming-gao
Zhao, Ming-gao
中科院分区:
医学2区
文献类型:
--
作者:
Li, Zi-lin;Liu, Jin-cheng;Zhao, Ming-gao

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民族药理意义:金丝桃苷(Hyperoside,Hyp)是从斜纹杜鹃叶中分离得到的一种具有体外血管保护作用的黄酮类化合物。Hyp可减轻氧化应激诱导的内皮细胞损伤,但其作用机制尚不清楚。本研究探讨了Hyp在过氧化氢(H_2O_2)诱导的内皮细胞损伤模型中的作用及其可能的机制。材料和方法:人脐静脉内皮细胞(HUVECs)用H_2O_2单独或与Hyp联合处理。结果:人脐静脉内皮细胞经400mM的H_2O_2作用18h后,细胞活力下降,细胞过度凋亡和死亡,而经Hyp处理的细胞凋亡和死亡明显减少。Western印迹分析显示,Hyp可上调Bcl2的表达,降低Bax的表达。此外,Hyp还诱导HUVEC中ERK1/2的磷酸化。结论:这些观察结果为Hyp至少部分地通过激活ERK信号通路来保护HUVEC免受过氧化氢损伤提供了初步证据。(C)2011爱思唯尔爱尔兰有限公司。保留所有权利。
Ethnopharmacological relevance: Hyperoside (Hyp) is a flavonoid compound isolated from Rhododendron ponticum L leaves that elicits vascular protective effects in vitro. Treatment with Hyp has been found to attenuate endothelial cell damage induced by oxidative stress, but its mechanisms of action remain unclear.This study investigated the action of Hyp in an endothelial injury model induced by hydrogen peroxide (H2O2), as well as its possible mechanisms.Materials and methods: Human umbilical vein endothelial cells (HUVECs) were treated with H2O2 alone or in combination with Hyp. The protective effects of Hyp against H2O2 were evaluated, and the activation of extracellular signal-regulated protein kinase (ERK) in Hyp was assayed in HUVECs.Results: Loss of cell viability as well as excessive cell apoptosis and death were observed in HUVECs after 18 h of challenge with H2O2 (400 mu M); however, both cell apoptosis and death were attenuated in the Hyp-pretreated cells. Western blot analysis revealed that Hyp increased the expression of Bcl-2 but decreased that of Bax. In addition, Hyp induced the phosphorylation of ERK1/2 in HUVECs.Conclusion: These observations provide preliminary evidence that Hyp protects HUVECs against H2O2 damage, at least partially, by activating the ERK signaling pathway. (C) 2011 Elsevier Ireland Ltd. All rights reserved.