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LPS诱导小鼠急性肺损伤TLR4及TNF-α表达

谷志龙 姜华茂 胡占升

中国医学创新Issue(24):16-19,4.
中国医学创新Issue(24):16-19,4.DOI:10.3969/j.issn.1674-4985.2015.24.006

LPS诱导小鼠急性肺损伤TLR4及TNF-α表达

Expression of Toll Like Receptor 4 and TNF-αon Acute Lung Injury Induced by Lipopolysaccharide in Mice

谷志龙 1姜华茂 1胡占升1

作者信息

  • 1. 辽宁医学院附属第一医院 辽宁 锦州 121001
  • 折叠

摘要

Abstract

Objective:To study mechanism of acute lung injury induced by lipopolysaccharide in mice.Method:The mice were randomly divided into normal control group,model group and antibody group.Control group was given 0.9%NaCl. Model group of acute lung injury was induced by LPS at a dose of 4 mg/kg. Aitibody group mice were given anti-TLR4/MD antibody (50μg)before 8-10 h of building model group. Blood and lung tissue were taken after modeling in 4 hours. A mount of endotoxin in plasma was measured by kinetic turbidimetric assay.Degree of lung damage was grated by HE staining. Expressions of TLR4 at both mRNA and protein levels were measured by RT-PCR and Western Blot.Content of TNF-αin mice serum was detected by ELISA.Result:Compared with the control group,endotoxin in serum,in model group and ayibody group significantly increased (P<0.05),with obvious ALI lung damages in model group.Compared with the model group,antibody group presented that expression of TLR4 mRNA and protein lower regulated(P<0.05)and ELISA results of TNF-αsignificantly decreased(P<0.05).Conclusion:The mechanism of acute lung injury induced by lipopolysaccharide may be related to TLR4 signal passway that mediates the TNF-αlevel.

关键词

脂多糖/急性肺损伤/Toll样受体4/肿瘤坏死因子-α

Key words

Lipopolysaccharide/ALI/Toll like receptor 4/TNF-α

引用本文复制引用

谷志龙,姜华茂,胡占升..LPS诱导小鼠急性肺损伤TLR4及TNF-α表达[J].中国医学创新,2015,(24):16-19,4.

基金项目

辽宁省教育厅课题 ()

中国医学创新

1674-4985

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