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Toll样受体3信号通路介导自身免疫性心肌炎炎症反应及作用机制

发布时间:2018-04-16 17:51

  本文选题:Toll样受体 + 信号通路 ; 参考:《免疫学杂志》2017年08期


【摘要】:目的探讨自身免疫性心肌炎大鼠心肌组织Toll样受体3(TLR3)表达水平及临床意义。方法将54只大鼠按照随机数字表法分为AM组、干预组和对照组,每组18只,对照组大鼠正常喂养,AM组、干预组建立自身免疫性心肌炎大鼠模型,干预组于模型建立第21天注射0.1 mg TLR3配体溶液,AM组、对照组大鼠注射等量PBS溶液。分别于模型建立第7、14、21、24、28、35天处死各组3只大鼠,观察各组大鼠心肌组织病理变化,酶联免疫吸附试验检测血清心肌肌凝蛋白自身抗体滴度,免疫组织化学染色法检测心肌组织TLR3蛋白表达,实时定量PCR检测心肌组织TLR3、TNF-αm RNA表达。结果对照组大鼠血清心肌肌凝蛋白自身抗体在不同时间点比较差异无统计学意义(P0.05),干预组血清心肌肌凝蛋白自身抗体滴度在第28天达高峰,AM血清心肌肌凝蛋白自身抗体滴度在第21天达高峰;第14、21、24、28、35天AM组、干预组血清心肌肌凝蛋白自身抗体滴度显著高于对照组(P0.05),第24、28、35天干预组血清心肌肌凝蛋白自身抗体滴度显著高于AM组(P0.05)。对照组TLR3蛋白表达在不同时间点比较差异无统计学意义(P0.05);第14、21、24、28、35天,AM组、干预组TLR3蛋白表达显著高于对照组(P0.05),第24、28、35天,干预组TLR3蛋白表达显著高于AM组(P0.05)。对照组TLR3、TNF-αm RNA相对表达量在不同时间点比较差异无统计学意义(P0.05);第7、14、21、24、28、35天,AM组、干预组TLR3、TNF-αm RNA相对表达量显著高于对照组(P0.05),第24、28、35天,干预组TLR3、TNF-αm RNA相对表达量显著高于AM组(P0.05)。结论自身免疫性心肌炎心肌组织TLR3表达上调,TLR3信号通路介导的炎症反应参与了自身免疫性心肌炎的发病。
[Abstract]:Objective to investigate the expression and clinical significance of Toll like receptor 3 (TLR3) in myocardium of rats with autoimmune myocarditis.Methods Fifty-four rats were randomly divided into AM group (n = 18), intervention group (n = 18) and control group (n = 18).The intervention group was injected with 0.1 mg TLR3 ligand solution on the 21st day and the control group was injected with the same amount of PBS solution.Three rats in each group were killed on day 7, 14, 21, 24, 2835, respectively. The pathological changes of myocardial tissue were observed and the autoantibody titers of serum myosin were detected by enzyme-linked immunosorbent assay (Elisa).The expression of TLR3 protein was detected by immunohistochemical staining and the expression of TLR3TNF- 伪 m RNA was detected by real-time quantitative PCR.Results there was no significant difference in serum myosin autoantibodies between control group and control group at different time points (P 0.05). The autoantibody titer of serum myocardial myosin in intervention group reached the peak on the 28th day, and the autoantibody titer of myocardial myosin in AM serum reached a peak on the 28th day.The titer of body antibody reached the peak on the 21st day.The titer of autoantibodies against myocardial myosin in the intervention group was significantly higher than that in the control group (P 0.05), and the titer of the autoantibody in the intervention group was significantly higher than that in the AM group on the 35th day.The expression of TLR3 protein in the control group was not significantly different at different time points, but the expression of TLR3 protein in the intervention group was significantly higher than that in the control group on day 2835, and the expression of TLR3 protein in the intervention group was significantly higher than that in the AM group.Conclusion the expression of TLR3 in myocardial tissue of autoimmune myocarditis may be involved in the pathogenesis of autoimmune myocarditis by upregulating the inflammatory response mediated by TLR3 signal pathway.
【作者单位】: 福建医科大学附属第二医院心内科;
【分类号】:R542.21

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相关期刊论文 前4条

1 叶迎春;年四季;刘佳佳;高燕;袁青;;IL-33与自身免疫疾病[J];中国免疫学杂志;2015年08期

2 徐玲;吕仕超;张军平;;Th17/Treg细胞失衡与自身免疫性心肌炎[J];中国免疫学杂志;2015年08期

3 樊z岩,

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