论文部分内容阅读
目的:探讨实验性自身免疫性心肌炎BALB/c小鼠模型心肌组织中Toll样受体3的表达变化及意义。方法:用猪心肌肌球蛋白诱导建立BALB/c小鼠自身免疫性心肌炎模型,心肌炎模型组(n=20)和poly(I∶C)干预组(n=24)小鼠于第0d和7d皮下注射猪心肌肌球蛋白和完全弗氏佐剂,对照组(n=18)小鼠相同时间仅注射完全弗氏佐剂。于初次免疫后的第14d和21d分别留取血清和心肌标本。HE染色光镜下观察心肌组织的炎症情况,间接ELISA法检测小鼠血清中抗肌球蛋白IgG抗体,采用免疫组织化学和实时-PCR检测心肌组织中Toll样受体3蛋白和mRNA的表达变化。结果:光镜下表现和血清学指标均提示心肌炎症;免疫组织化学显示Toll样受体3在实验性自身免疫性心肌炎模型中有表达;在poly(I∶C)注射12h后Toll样受体3mRNA表达量最高,约为基础表达量的20倍,显著差异(P<0.05),且呈时间依赖性;心肌炎模型组中干扰素β和肿瘤坏死因子αmRNA表达与正常对照组比较分别增加14倍和18倍,显著差异(P<0.05)。结论:自身免疫性心肌炎小鼠心肌中Toll样受体3表达增加,其诱导的炎症反应与Toll样受体3介导的信号转导通路有关。
Objective: To investigate the changes and significance of Toll-like receptor 3 in myocardium of BALB / c mouse model of experimental autoimmune myocarditis. Methods: BALB / c mouse models of autoimmune myocarditis induced by porcine cardiac myosin were established in the myocarditis model group (n = 20) and poly (I: C) intervention group Subcutaneous injection of porcine myocardium myosin and complete Freund’s adjuvant, control (n = 18) mice were injected with complete Freund’s adjuvant only at the same time. Serum and myocardial samples were collected on the 14th and 21st day after the first immunization. The inflammation of myocardial tissue was observed under HE staining and the anti-myosin IgG antibody in serum was detected by indirect ELISA. The expression of Toll-like receptor 3 protein and mRNA in myocardium was detected by immunohistochemistry and real-time-PCR . RESULTS: Myocardial inflammation was detected by light microscopy and serological markers. Immunohistochemistry showed that Toll-like receptor 3 was expressed in experimental autoimmune myocarditis model. Toll-like receptor 3 mRNA was the highest, about 20-fold higher than the basal expression (P <0.05), and in a time-dependent manner. The levels of IFN-α and TNF-αmRNA in myocarditis model group were increased by 14-fold compared with the normal control group And 18-fold, significant difference (P <0.05). CONCLUSION: The expression of Toll-like receptor 3 in myocardium of mice with autoimmune myocarditis is increased, and the inflammatory response induced by Toll-like receptor 3 is related to the signal transduction pathway.