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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

曾慰 肖新华 胡名松 邓宏军 胡军 郑达扬 高文奎

中国动脉硬化杂志2011,Vol.19Issue(7):552-556,5.
中国动脉硬化杂志2011,Vol.19Issue(7):552-556,5.

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

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

曾慰 1肖新华 2胡名松 1邓宏军 1胡军 1郑达扬 1高文奎1

作者信息

  • 1. 南华大学附属第二医院胸外科,湖南省衡阳市421001
  • 2. 南华大学附属第一医院内分泌实验室,湖南省衡阳市421001
  • 折叠

摘要

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-1 β 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-1 β 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.

关键词

叔丁基对苯二酚/转录因子NF-E2相关因子2/脂多糖/人脐静脉内皮细胞

Key words

Tert-Butylhydroquinone/ Nuclear Factor-Erythroid 2 p45-Related Factor 2/ Lipoppolysacchride/ Human Umbilial Vein Endothelial Cell

分类

医药卫生

引用本文复制引用

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):552-556,5.

基金项目

国家自然科学基金(81070667) (81070667)

中国动脉硬化杂志

OA北大核心CSCDCSTPCD

1007-3949

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