尿酸减轻氧化应激诱导的血管内皮细胞损伤
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Uric Acid Attenuates Oxidative Stress-Induced Injury in Vascular Endothelial Cells
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    目的 探讨尿酸对氧化应激情况下的人脐静脉内皮细胞(HUVEC)有无保护作用以及其可能的机制。方法 将人脐静脉内皮细胞分为四组:不做任何处理的对照组、单纯叔丁基过氧化氢(t-BHP)组、单纯尿酸组和尿酸+t-BHP组。MTT试验计算各组细胞存活率。DCFH-DA探针检测各组细胞内活性氧(ROS)水平。流式细胞仪检测各组细胞凋亡情况。荧光定量PCR技术检测各组细胞核转录相关因子2(Nrf2)mRNA表达变化。Western blot 技术检测各组细胞胞浆与胞核中Nrf2蛋白表达水平。结果 MTT试验发现,尿酸+t-BHP组细胞存活率(78.5%±7.6%)显著高于单纯t-BHP组(P<0.05)。尿酸+t-BHP组细胞内ROS水平以及细胞凋亡率都明显低于单纯t-BHP组(P<0.05)。各组Nrf2的mRNA表达水平差异均无显著性(P>0.05),但单纯尿酸组与尿酸+t-BHP组细胞核内Nrf2明显增多。结论 尿酸对氧化应激下的血管内皮细胞具有保护作用,其机制可能为尿酸增加了血管内皮细胞中Nrf2的核内转移。

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    Aim To explore the protective effect of uric acid on human umbilical vein endothelial cell (HUVEC) injury induced by oxidative stress and its underlying mechanism. Methods HUVEC were divided into four groups: control group,tert-butyl hydroperoxide (t-BHP)-treated group,uric acid-treated group,t-BHP plus uric acid-treated group.Cell viability was evaluated by MTT assay.Intracellular reactive oxygen species (ROS) level was detected by DCFH-DA fluorescence probe.Cell apoptosis was determined by flow cytometry.NF-E2-related factor 2 (Nrf2) expressions in the mRNA and protein level were analyzed by qRT-PCR and Western blot,respectively. Results t-BHP treatment caused significant decline in cell viability of HUVEC,which was attenuated by uric acid treatment.Moreover,intracellular ROS level was down-regulated in t-BHP plus uric acid-treated group compared with t-BHP-treated group.Cell apoptosis rate exhibited similar trend.All four groups exhibited similar Nrf2 mRNA level.However,the nuclear translocation of Nrf2 was elevated significantly in both uric acid-treated group and t-BHP plus uric acid-treated group. Conclusions Uric acid could prevent HUVEC from oxidative stress possibly via Nrf2 nuclear translocation and activation.

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孙海斌.尿酸减轻氧化应激诱导的血管内皮细胞损伤[J].中国动脉硬化杂志,2014,22(10):1019~1022.

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  • 收稿日期:2014-02-19
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