中国医学创新
中國醫學創新
중국의학창신
MEDICAL INNOVATION OF CHINA
2015年
24期
16-19
,共4页
脂多糖%急性肺损伤%Toll样受体4%肿瘤坏死因子-α
脂多糖%急性肺損傷%Toll樣受體4%腫瘤壞死因子-α
지다당%급성폐손상%Toll양수체4%종류배사인자-α
Lipopolysaccharide%ALI%Toll like receptor 4%TNF-α
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50μg。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。
目的：研究脂多糖（LPS）誘導的小鼠急性肺損傷機製。方法：實驗分為正常對照組、模型組及抗體組；正常對照組小鼠腹腔腔內註射等量0.9%NaCl。模型組腹腔內註射LPS（4 mg/kg）。抗體組在造模前8~10 h，應用小鼠Toll樣受體4/髓樣分化蛋白2（TLR4/MD2）複閤物抗體腹腔內註射50μg。各組均在造模5 h後留取血和肺組織，採用細菌內毒動態濁度法檢測血漿LPS的含量，HE染色判定小鼠肺組織病理變化，RT-PCR測定小鼠肺組織TLR4基因錶達，Western-blot測定TLR4蛋白錶達；ELISA檢測小鼠血清中TNF-α的水平。結果：和正常對照組比較，模型組及抗體組小鼠血漿內毒素含量顯著升高（P<0.05），模型組小鼠肺組織HE染色呈ALI錶現；和模型組比較，抗體組TLR4 mRNA、蛋白及TNF-α的錶達明顯下調（P<0.05）。結論：急性肺損傷機製可能與LPS和TLR4受體結閤介導TNF-α信號途徑相關。
목적：연구지다당（LPS）유도적소서급성폐손상궤제。방법：실험분위정상대조조、모형조급항체조；정상대조조소서복강강내주사등량0.9%NaCl。모형조복강내주사LPS（4 mg/kg）。항체조재조모전8~10 h，응용소서Toll양수체4/수양분화단백2（TLR4/MD2）복합물항체복강내주사50μg。각조균재조모5 h후류취혈화폐조직，채용세균내독동태탁도법검측혈장LPS적함량，HE염색판정소서폐조직병리변화，RT-PCR측정소서폐조직TLR4기인표체，Western-blot측정TLR4단백표체；ELISA검측소서혈청중TNF-α적수평。결과：화정상대조조비교，모형조급항체조소서혈장내독소함량현저승고（P<0.05），모형조소서폐조직HE염색정ALI표현；화모형조비교，항체조TLR4 mRNA、단백급TNF-α적표체명현하조（P<0.05）。결론：급성폐손상궤제가능여LPS화TLR4수체결합개도TNF-α신호도경상관。
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.
