tBHQ通过Nrf2通路抗脂多糖诱导人脐静脉内皮细胞损伤中的作用及机制
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国家自然科学基金(81070667)


Effects of tBHQ on Lipoppolysacchride-Induced Impairment of Human Umbilial Vein Endothelial Cell by Nuclear Factor-Erythroid 2 p45-Related Factor 2
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    摘要:

    目的探讨叔丁基对苯二酚(tBHQ)在抗脂多糖诱导人脐静脉内皮损伤中的作用及相关机制。方法体外培养人脐静脉内皮细胞,用脂多糖作用建立人脐静脉内皮损伤模型前,用不同浓度叔丁基对苯二酚预处理24h。用MTT法检测内皮细胞活性,Western blot检测细胞核内和核外转录因子NF-E2相关因子2(Nrf2)蛋白表达,DCFH-DA染色法检测细胞内活性氧量,Western blot和ELISA检测肿瘤坏死因子α、白细胞介素1β和白细胞介素6水平。结果与对照组相比,脂多糖处理能够显著降低细胞活性,而叔丁基对苯二酚能够显著抑制脂多糖的损伤作用(P<0.05)。与脂多糖单独处理组相比,叔丁基对苯二酚预处理能够显著增加核内Nrf2蛋白水平,并显著降低活性氧、肿瘤坏死因子α、白细胞介素1β和白细胞介素6水平(P<0.05)。结论叔丁基对苯二酚能够通过诱导Nrf2的核转位来抑制脂多糖诱导的活性氧和炎症因子增加,起到抗内皮细胞损伤作用。

    Abstract:

    Aim To investigate the role and mechanism of tert-butylhydroquinone(tBHQ) on lipoppolysacchride(LPS)-induced impairment of human umbilial vein endothelial cell(HUVEC).Methods Before treated with LPS,HUVEC were cultured with tBHQ in vitro.MTT analysis measured the effects of LPS and tBHQ on HUVEC;Western blot analysis measured the effects of tBHQ on the levels of Nrf2 in HUVEC;DCFH-DA measured the effects of tBHQ on the levels of ROS;Western blot and ELISA analysis measured the effects of tBHQ on the levels of TNF-α,IL-1β and IL-6.Results Compared with control group,viabilities of HUVEC were decreased significantly by LPS(P<0.05).However,the effects of LPS could be attenuated notably by tBHQ(P<0.05).Pretreatment with tBHQ could increase the expression of nuclear Nrf2 protein significantly(P<0.05),and reduce the levels of ROS,TNF-α,IL-1β and IL-6(P<0.05).Conclusions To prevent LPS-induced impairment of HUVEC,tBHQ can decrease the levels of ROS inflammatory factors induced by LPS via inducing translocation of Nrf2.

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曾 慰, 肖新华, 胡名松, 邓宏军, 胡 军, 郑达扬, 高文奎. tBHQ通过Nrf2通路抗脂多糖诱导人脐静脉内皮细胞损伤中的作用及机制[J].中国动脉硬化杂志,2011,19(7):552~556.

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  • 收稿日期:2011-05-18
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