TLR4、MyD88、NF-κBmRNA在实验性自身免疫性肌炎小鼠淋巴结中的表达及意义  

The expression and significance of TLR4,MyD88 and NF-кB mRNA in mouse lymph node of experimental autoimmune myositis

作　　者：张红鸭[1] 康娟 韩文娟[1] 胡萌萌[1] 贾宏阁[1] 

机构地区：[1]第四军医大学西京医院神经内科,陕西西安710032 [2]清涧县医院,陕西榆林718300

出　　处：《细胞与分子免疫学杂志》2012年第3期272-275,共4页Chinese Journal of Cellular and Molecular Immunology

基　　金：国家自然科学基金资助项目(81171181)

摘　　要：目的:研究TLR4、MyD88、NF-κB mRNA在实验性自身免疫性肌炎小鼠淋巴结中的表达情况,探讨TLR4在肌炎发病中的作用。方法:将30只雌性BALB/c小鼠随机分为5组(每组6只):第1组为正常对照组,其它4组分别为肌炎模型1周处理组、2周处理组、3周处理组和4周处理组,后4组均应用肌球蛋白诱导实验性自身免疫性肌炎模型(EAM)。采用实时荧光定量PCR方法检测各组小鼠淋巴结TLR4、MyD88、NF-κB mRNA表达水平。结果:(1)与正常小鼠相比,肌炎各组小鼠淋巴结中TLR4、MyD88、NF-κB mRNA表达均有统计学差异,表现为不同程度升高(P<0.01),第3组升高最为显著(P<0.01),第4组较第5组升高(P<0.01);(2)各组淋巴结中TLR4 mRNA表达水平与MyD88 mRNA、NF-κBmRNA表达水平均呈正相关(r=0.906,r=0.967,P<0.01),MyD88 mRNA表达水平与NF-κB mRNA表达水平呈正相关(r=0.919,P<0.01)。结论:TLR4在自身免疫性肌炎发生发展过程中发挥重要作用,且以MyD88依赖型信号途径为主,并通过激活NF-κB促进炎性因子释放。AIM： To investigate TLR4,MyD88 and NF-кB mRNA levels in mouse lymph node with experimental autoimmune myositis（EAM）and determine the role of TLR4 in autoimmune myositis.METHODS： Thirty femal BALB/c mice were randomly divided into five groups（n=6 animals per group）： group 1 was the control,while animals in other four groups were killed at different time point： group 2 in the first week,group 3 in the second week,group 4 in the third week and group 5 in the fourth week since they had been given myosin for preparing EAM.The expressions of TLR4,MyD88 and NF-κB mRNA were measured with real-time fluorescent quantitative polymerase chain reaction.RESULTS：（1）The expressions of TLR4,MyD88 and NF-κB mRNA in each EAM group were significantly high compared with those in the normal control group,which was significantly highest in group 3 of all（P〈0.01） and significantly higher in group 4 than in group 5（P〈0.01）.（2）The expression level of TLR4 mRNA had significant positive correlations with the expressions of MyD88 mRNA and NF-κB mRNA（r=0.906,r=0.967,P〈0.01）,and the latter two also had significant positive correlations（r=0.919,P〈0.01）.CONCLUSION： TLR4 played an important role in the development of autoimmune myositis and run its function mainly by MyD88-dependent pathway that could activate NF-κB for promoting the release of inflammatory factors.

关 键 词：实验性自身免疫性肌炎 TLR4 MYD88 NF-ΚB 

分 类 号：R392.11[医药卫生—免疫学]