Toll样受体3在自身免疫性心肌炎小鼠心肌组织中的表达及意义  

Expression of Toll-like receptor 3 in myocardium in experimental autoimmune myocarditis

作　　者：田青[1] 周恒[1] 王蕾[1] 甘文云[1] 郭海鹏[1] 姜明[2] 邓伟[3] 艾文[1] 卞洲艳[1] 严玲[1] 沈涤非[1] 唐其柱[1] 

机构地区：[1]武汉大学人民医院心内科,武汉大学心血管病研究所,湖北武汉430060 [2]安庆市立医院心内科,安徽安庆246003 [3]荆州市中心医院心内科,湖北荆州434020

出　　处：《中国病理生理杂志》2009年第12期2323-2328,共6页Chinese Journal of Pathophysiology

摘　　要：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。AIM： To establish an animal model of experimental autoimmune myocarditis （EAM） in BALB/c mice and to investigate the expression and significance of Toll - like receptor 3 in mouse EAM. METHODS： BALB/c mice were immunized with cardiac myosin extracted from porcine ventricnlar myocardium covered by complete freund＇s adjuvant （CFA） on 0 d and 7 d, then divided into EAM group （n =20） and poly （I： C） group （n =24）. Control mice （n = 18） were immunized with CFA only. Serum and myocardium samples were collected at 14 d and 21 d after the first immunization. HE staining was used to identify the areas of inflammation. The myosin IgG antibody was examined by indirect ELISA assay. The changes of TLR3 protein and mRNA expression in myocardial tissue were measured by immunohistochemistry and real time - PCR. RESULTS： Compared to control group, immunohistochemistry results showed that there was positive expression of TLR3 in the myocardium of mice with EAM and the mRNA of TLR3 were more than 20 times increased in a time - dependent manner at 12 h after poly （ I ： C ） injection （ P 〈 0. 05 ）. The expression of interferon beta mRNA in EAM group was more than 14 times as many as basal expression, that of tumor necrosis factor alpha was more than 18 times （ P 〈 0. 05 ）. CONCLUSION ： The expression of Toll - like receptor 3 in mvocardium is up - regulated in experimental autoimmune myocarditis. The inflammatory response to cardiac myosin may associate with the TLR3 signal transduction pathway.

关 键 词：受体 Toll样 细胞因子类 心肌炎 自身免疫性 心肌病 充血性 

分 类 号：R542.2[医药卫生—心血管疾病]