2024年4月17日发(作者：系千易)
LPS诱导小鼠急性肺损伤TLR4及TNF―α表达
【摘要】 目的：研究脂多糖（LPS）诱导的小鼠急性肺损伤机制。方法：实验分为正
常对照组、模型组及抗体组；正常对照组小鼠腹腔腔内注射等量0.9%NaCl。模型组腹腔
内注射LPS（4 mg/kg）。抗体组在造模前8～10 h，应用小鼠Toll样受体4/髓样分化蛋
白2（TLR4/MD2）复合物抗体腹腔内注射50 μg。各组均在造模5 h后留取血和肺组织，
采用细菌内毒动态浊度法检测血浆LPS的含量，HE染色判定小鼠肺组织病理变化，RT-PCR
测定小鼠肺组织TLR4基因表达，Western-blot测定TLR4蛋白表达；ELISA检测小鼠血
清中TNF-α的水平。结果：和正常对照组比较，模型组及抗体组小鼠血浆内毒素含量显著
升高（P<0.05），模型组小鼠肺组织HE染色呈ALI表现；和模型组比较，抗体组TLR4
mRNA、蛋白及TNF-α的表达明显下调（P<0.05）。结论：急性肺损伤机制可能与LPS和
TLR4受体结合介导TNF-α信号途径相关。
【关键词】 脂多糖； 急性肺损伤； Toll样受体4； 肿瘤坏死因子-α
Expression of Toll Like Receptor 4 and TNF-α on Acute Lung Injury Induced by
Lipopolysaccharide in Mice/GU Zhi-long，JIANG Hua-mao，HU
Zhan-sheng.//Medical Innovation of China，2015，12（24）：016-019
【Abstract】 Objective：To study mechanism of acute lung injury induced by
lipopolysaccharide in ：The mice were randomly divided into normal
control group， model group and antibody l 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（50 μg） 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
of lung damage was grated by HE staining. Expressions of TLR4 at
both mRNA and protein levels were measured by RT-PCR and Western
t of TNF-α in mice serum was detected by ：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
ed with the model group， antibody group presented that
expression of TLR4 mRNA and protein lower regulated（P<0.05） and ELISA results
of TNF-α significantly 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-α level.
【Key words】 Lipopolysaccharide； ALI； Toll like receptor 4； TNF-α
First-author’s address：The First Affiliated Hospital of Liaoning Medical
College，Jinzhou 121001，China
doi：10.3969/.1674-4985.2015.24.006
急性肺损伤（Acute Lung Injury，ALI）是在创伤、重症感染、休克等等非心源性疾
病过程中，肺泡上皮细胞和肺毛细血管内皮细胞损伤造成的弥漫性肺间质及肺泡水肿，导
致的急性低氧性呼吸功能不全或衰竭[1]；脂多糖（LPS）诱导的ALI在重症感染后早期出
现[2]，并且死亡率较高[3]。Toll like receptors（TLRs）家族和先天性免疫系统关系比较
密切[4]，其中TLR4目前研究最多，是LPS受体[5]。本实验基于建造小鼠内毒诱导ALI[6-7]，
深入探讨ALI、LPS和TLR4及TNF-α之间的关系及损伤机制，并可能为临床ALI的预防
2024年4月17日发(作者：系千易)
LPS诱导小鼠急性肺损伤TLR4及TNF―α表达
【摘要】 目的：研究脂多糖（LPS）诱导的小鼠急性肺损伤机制。方法：实验分为正
常对照组、模型组及抗体组；正常对照组小鼠腹腔腔内注射等量0.9%NaCl。模型组腹腔
内注射LPS（4 mg/kg）。抗体组在造模前8～10 h，应用小鼠Toll样受体4/髓样分化蛋
白2（TLR4/MD2）复合物抗体腹腔内注射50 μg。各组均在造模5 h后留取血和肺组织，
采用细菌内毒动态浊度法检测血浆LPS的含量，HE染色判定小鼠肺组织病理变化，RT-PCR
测定小鼠肺组织TLR4基因表达，Western-blot测定TLR4蛋白表达；ELISA检测小鼠血
清中TNF-α的水平。结果：和正常对照组比较，模型组及抗体组小鼠血浆内毒素含量显著
升高（P<0.05），模型组小鼠肺组织HE染色呈ALI表现；和模型组比较，抗体组TLR4
mRNA、蛋白及TNF-α的表达明显下调（P<0.05）。结论：急性肺损伤机制可能与LPS和
TLR4受体结合介导TNF-α信号途径相关。
【关键词】 脂多糖； 急性肺损伤； Toll样受体4； 肿瘤坏死因子-α
Expression of Toll Like Receptor 4 and TNF-α on Acute Lung Injury Induced by
Lipopolysaccharide in Mice/GU Zhi-long，JIANG Hua-mao，HU
Zhan-sheng.//Medical Innovation of China，2015，12（24）：016-019
【Abstract】 Objective：To study mechanism of acute lung injury induced by
lipopolysaccharide in ：The mice were randomly divided into normal
control group， model group and antibody l 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（50 μg） 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
of lung damage was grated by HE staining. Expressions of TLR4 at
both mRNA and protein levels were measured by RT-PCR and Western
t of TNF-α in mice serum was detected by ：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
ed with the model group， antibody group presented that
expression of TLR4 mRNA and protein lower regulated（P<0.05） and ELISA results
of TNF-α significantly 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-α level.
【Key words】 Lipopolysaccharide； ALI； Toll like receptor 4； TNF-α
First-author’s address：The First Affiliated Hospital of Liaoning Medical
College，Jinzhou 121001，China
doi：10.3969/.1674-4985.2015.24.006
急性肺损伤（Acute Lung Injury，ALI）是在创伤、重症感染、休克等等非心源性疾
病过程中，肺泡上皮细胞和肺毛细血管内皮细胞损伤造成的弥漫性肺间质及肺泡水肿，导
致的急性低氧性呼吸功能不全或衰竭[1]；脂多糖（LPS）诱导的ALI在重症感染后早期出
现[2]，并且死亡率较高[3]。Toll like receptors（TLRs）家族和先天性免疫系统关系比较
密切[4]，其中TLR4目前研究最多，是LPS受体[5]。本实验基于建造小鼠内毒诱导ALI[6-7]，
深入探讨ALI、LPS和TLR4及TNF-α之间的关系及损伤机制，并可能为临床ALI的预防