论文摘要
目的：研究Smad7在胶原诱导性关节炎（collagenⅡ-induced arthritis,CIA）中的作用以及可能机制。方法：利用Smad7基因敲除（Smad7-KO）和野生型（Smad7-WT）的小鼠,建立CIA模型,分为疾病组（CIA-KO/WT）、对照组（CTL-KO/WT）及正常组（Nor-KO/WT）共6组,通过观察小鼠大体情况、病理形态和通过免疫组化（IHC）、酶联免疫吸附测定（Elisa）及实时聚合酶链反应（RT-PCR）等途径对比各组的多种疾病指标。结果：和正常组相比,CIA-KO组的小鼠关节肿胀程度明显加重,滑膜增生、关节软骨破坏；免疫组化显色提示炎症反应（CD3、F4/80、TNFα、MCP-1、IL-1、T-bet）增强、TGF-β1信号途径（TGF-β、P-Smad2/3）、NF-κB途径（P-P65）激活；Elisa方面显示血浆IL-17A与抗CⅡ抗体IgG、IgG1、IgG2a水平上升；RT-PCR方面显示TNFα、IL-1、T-bet、IL-6、RORγt、IL-17等mRNA增高,且各个指标与对照组相比都有显著性差异。结论：提示Smad7的缺失加重关节炎,机制可能与Smad7的缺失减少了对NF-κB与TGF-β的抑制,增加NF-κB与TGF-β信号通路,并促进Th17分化,从而导致免疫紊乱与加重炎症反应有关。
论文目录
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