去甲肾上腺素减轻脂多糖所致内皮细胞损伤  

Norepinephrine attenuates injury of vascular endothelial cells induced by LPS

作　　者：胡静[1] 龙燕琼[1] 岳阳[1] 刘作良[1] HU Jing;LONG Yan-qiong;YUE Yang;LIU Zuo-liang(The Third Xiangya Hospital,Central South University,Changsha 410013,China)

机构地区：[1]中南大学湘雅三医院,湖南长沙410013

出　　处：《中国病理生理杂志》2018年第4期735-738,共4页Chinese Journal of Pathophysiology

基　　金：湖南省卫生计生委科研计划课题项目(No.C2017005)

摘　　要：目的:探讨去甲肾上腺素(norepinephrine,NE)减轻脂多糖(lipopolysaccharides,LPS)对内皮细胞损伤的作用。方法:用100 mg/L LPS诱导人脐静脉血管内皮细胞HUVEC-12损伤,用不同浓度NE处理后,使用realtime PCR及Western blot法检测各组内皮细胞血管内皮型钙黏素(VE-cadherin)表达的变化,ELISA法测定细胞培养上清液中TNF-α、IL-1β、IL-2和IL-10的浓度,活性氧簇(reactive oxygen species,ROS)检测试剂盒检测细胞内的ROS水平。结果:LPS可显著抑制内皮细胞中VE-cadherin m RNA和蛋白的表达水平,同时伴有TNF-α、IL-1β和IL-2升高及IL-10下降,ROS含量明显增加;不同浓度的NE呈剂量依赖性地上调VE-cadherin的m RNA和蛋白表达,减轻细胞内的氧化应激水平,并部分逆转TNF-α、IL-1β、IL-2和IL-10的变化。结论:不同浓度NE能明显逆转LPS造成的内皮细胞损伤,其机制可能与上调VE-cadherin、减轻细胞的氧化应激及炎性介质水平有关。AIM:To investigate the effects of norepinephrine(NE)on vascular endothelial cell damage induced by lipopolysaccharides(LPS).METHODS:Human umbilical vein endothelial cells(HUVEC-12)were cultured with LPS at 100 mg/L to establish the cell damage model.Real-time PCR and Western blot were used to determine the expressions of VE-cadherin at mRNA and protein levels.The levels of TNF-α,IL-1β,IL-2 and IL-10 in culture supernatant were measured by ELISA.The reactive oxygen species(ROS)production in the endothelial cells was detected by ROS assay kit.RESULTS:LPS decreased both mRNA and protein levels of VE-cadherin accompanied by increased levels of TNF-α,IL-1β,IL-2 and intracellular ROS,and decreased level of IL-10 in the endothelial cells.NE reversed the expression of VE-cadherin at mRNA and protein levels under the condition of LPS treatment in a dose-dependent manner,and also alleviated the intracellular oxidative stress.CONCLUSION:NE reverses the endothelial damage induced by LPS,which may be related to the up-regulation of VE-cadherin level and the decreases in oxidative stress and inflamatory mediators.

关 键 词：去甲肾上腺素 脂多糖 内皮损伤 脓毒症 

分 类 号：R363.2[医药卫生—病理学] R631[医药卫生—基础医学]