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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。
Objective: To investigate the expression of TLR4, MyD88 and NF-κB mRNA in the lymph nodes of mice with experimental autoimmune myositis and to explore the role of TLR4 in the pathogenesis of myositis. Methods: Thirty female BALB / c mice were randomly divided into 5 groups (6 in each group): the first group was the normal control group, the other four groups were the myositis model 1 week treatment group, the 2 week treatment group 3 Weekly treatment group and 4 weeks treatment group, the latter four groups were used myosin induced experimental autoimmune myositis model (EAM). Real-time quantitative PCR was used to detect the expression of TLR4, MyD88 and NF-κB mRNA in lymph nodes in each group. Results: (1) Compared with normal mice, the expression of TLR4, MyD88 and NF-κB mRNA in lymph nodes of mice with myositis showed statistically significant difference (P <0.01), while in group 3 (P <0.01). (2) The expression of TLR4 mRNA in lymph nodes of each group was positively correlated with the expression of MyD88 mRNA and NF-κB mRNA (r = 0.906, r = 0.967, P <0.01). MyD88 mRNA expression was positively correlated with NF-κB mRNA expression (r = 0.919, P <0.01). CONCLUSION: TLR4 plays an important role in the development and progression of autoimmune myositis. MyD88-dependent signaling pathway is the main pathway and promotes the release of inflammatory cytokines by activating NF-κB.