痹清饮对类风湿关节炎活动期T细胞免疫调控机理研究
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摘要
目的:研究类风湿关节炎(RA)的病因病机,探讨痹清饮抗RA的细胞免疫调控机理,在细胞分子水平上,为中药制剂抗RA的临床应用和进一步的药理研究提供科学依据。方法:以Jurkat细胞为模型,以白芍总苷(TGP)、地塞米松(DEX)、甲氨蝶呤(MTX)为对照药物,采用流式细胞仪、MTT、ELISA免疫学方法,观察痹清饮对Jurkat细胞的增殖、分化、周期的影响;对RA患者外周血中T淋巴细胞活化作用的影响。结果:痹清饮可抑制T淋巴细胞的增殖、CD69、CD25的表达,下调IL-2的产生和IFN-γ的表达,与模型组对照有显著性差异(p<0.01 or p<0.05),与TGP\DEX\MTX组对照无显著性差异(p>0.05)。痹清饮还可使Jurkat细胞Gl期阻滞,Gl期细胞堆积,不能进入S期,阻滞Gl期向S期转化进程,从而使G2/M期细胞相对增多。结论:痹清饮对RA的细胞免疫调控机制可能是:通过抑制T细胞的活化,下调IL-2和IFN-γ的产生间接抑制Th分化增殖,从而减轻关节或/和滑膜的炎症反应和增生,减慢骨质破坏的进程;通过阻止T细胞能量和原料合成,减少细胞向G2期的转化,促进了异常增生的滑膜细胞凋亡的发生。
Objective: To study epidemiology and pathogenesis of rheumatoid arthritis (RA) in TCM, and Study on the pharmacological mechanisms on cellular immunity of BiQingYin for the treatment of Rheumatoid Arthritis. Scientific evidence of this research would make TCM on treatment on developed further. Methods: As the classical experimental model of T Lymphocytes, Jurkat cell was used to study the pharmacological mechanisms on cellular immunity of BiQingYin for the treatment of Rheumatoid Arthritis. Select TGP, MTX, and DEX as the control group. Investigate the effection of cellular immunity on activation ,differentiation, proliferation, cell cycle and signal molecule of T lymphocytes whish played a important in RA pathological process with immunological methods like flow cytometry, MTT and ELISA.Results: BiQingYin could inhibite the proliferation of Jurkat cell, down-regulated the levels of cytokine IL-2 and IFN-γby activated T cells, down-regulated the expression of CD69 and CD25 expressed on T lymphocytes in peripheral blood mononuclear cells from RA. It showed significant different in BiQingYin group and the model group (p<0.01 or p<0.05) and showed insignificant different (p>0.05) in BiQingYin group and the control group. FACS assay showed that the G1 term was prolonged by high and moderate doses of BiQingYin. Conclusion:The pharmacological mechanisms on cellular immunity of BiQingYin for the treatment of Rheumatoid Arthritis is related to inhibit the activation ,differentiation, proliferation, cell cycle and signal molecule of T lymphocytes
引文
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