浸润性T淋巴细胞表达IRF-7对骨性关节炎微环境的调控作用与补肾活血中药干预的研究

骨性关节炎（OA）的发病与机体微环境密切相关，局部炎症反应可促使滑液增加、骨损伤加重和疼痛增强。T淋巴细胞受机体抗原递呈细胞调控，骨关节炎患者T淋巴细胞被激活侵入到关节中，发挥着免疫炎症功能，而高度浸润T淋巴细胞释放大量炎症因子，促进关节炎发生和恶化程度增加。本课题基于OA患者中浸润性T淋巴细胞异常激活，受自身免疫诱导产生的IFN-α/β作用，激活浸润性T淋巴细胞表达关键的干扰素调节因子7，炎症因子信号通路磷酸化IRF-7，活化NF-κβ促使白介素6表达，从而介导骨性关节炎微环境恶化的这一假说，研究OA内浸润性T淋巴细胞活化并表达IRF-7，分析其磷酸化激活NF-κβ信号，从而明确IL-6表达活化而激活Jagged-Notch信号导致微环境改变和恶化，研究补肾活血中药抑制IRF-7表达及对其分子机制的作用，抑制这一微环境恶化进程，有利于明确该中药逆转OA的分子机制，为中药防治OA提供基础。

The incidence of osteoarthritis (OA) is closely related to the body microenvironment.Its local inflammatory response prompted synovial deterioration, bone injury aggravation and pain increase. T lymphocytes maintain the immune balance by regulatory role of antigen persenting cells. OA patients activated T lymphocytes which infiltrate into synovial fluid, and play the function of immune inflammation, so that arthritis occurs and its deteriorated degree is increased. The subject is based on the abnormal activation of infiltrating T lymphocytes in OA patients. With the role of IFN-alpha/beta induecd by self-immunine, infiltrating T lymphocytes were activated and expressed key interferon regulatory factor 7.Inflammatory factor signaling pathways phosphorylated IRF - 7, and activated the NF-κβwhich prompted expression of interleukin 6,so mediated by degradation of microenvironment in OA.We will research abnormal activation of infiltrating T lymphocytes and express the IRF - 7 and analyze its phosphorylation to activate NF-κβsignaling. So we confirm activation of IL - 6 expression to activate Jagged - Notch signal, resulting from regulating environmental change and degradation.We will research nourishing kidney and activating blood recipe which inhibit IRF - 7 expression and the role of its molecular mechanism,so inhibit chondrocyte worsening course. Therefore it confirms molecular mechanism of reversal role of the traditional Chinese medicine and theory of TCM prevention in OA.