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目的探讨复方雷公藤外敷治疗类风湿关节炎的可能作用机制。方法 30只SD大鼠随机分为正常组、模型组和雷公藤外敷组,每组10只。除正常组外其余两组采用Ⅱ型胶原诱导型关节炎大鼠模型,雷公藤外敷组于首次免疫后第14天起,大鼠双后肢给予复方雷公藤外敷剂0.50 g/(kg·d)外敷,每天1次,连续28天,模型组、正常组不给予处理。每周测量各组大鼠后足体积,实验结束时检测血清及滑膜组织白细胞介素1β(IL-1β)、肿瘤坏死因子α(TNF-α)、血管内皮生长因子(VEGF)和血管生成素1(Ang-1)含量以及滑膜组织细胞外信号调节激酶(ERK)通路蛋白表达,并进行关节病理检测。结果模型组大鼠后足体积、血清(除VEGF外)及滑膜组织各细胞因子水平较正常组明显升高,滑膜组织p-ERK1/2表达亦升高(P<0.05或P<0.01),关节病理切片显示可见大量炎症细胞浸润,关节软骨及关节面严重破坏,骨实质侵蚀,结构紊乱。而复方雷公藤外敷组大鼠血清IL-1β、TNF-α和Ang-1水平降低,滑膜组织中各细胞因子水平及mRNA表达下降,p-ERK1/2表达降低(P<0.05或P<0.01);病理显示复方雷公藤外敷有良好的抑制滑膜组织增殖、减少炎症细胞浸润、延缓骨与软骨破坏的效果。结论复方雷公藤外敷剂可能通过降低关节炎滑膜组织炎症细胞因子水平、减弱ERK通路活化,从而抑制滑膜组织增殖、减少滑膜中血管新生和血管翳形成。
Objective To investigate the possible mechanism of Compound Tripterygium wilfordii for the treatment of rheumatoid arthritis. Methods Thirty SD rats were randomly divided into normal group, model group and tripterygium wilfordii external application group, with 10 rats in each group. Except for the normal group, the rats in the other two groups were treated with type Ⅱ collagen induced arthritis. Tripterygium wilfordii external application group was given 14 days after the first immunization, and the rats’ hindlimbs were given compound triptolide 0.50 g / (kg · d) Topical application, once a day, for 28 consecutive days, the model group, the normal group did not give treatment. The hind paw volume of rats in each group was measured weekly. IL-1β, TNF-α, VEGF and angiogenesis in serum and synovial tissue were measured at the end of the experiment. Ang-1 and synovial tissue extracellular signal-regulated kinase (ERK) pathway protein expression, and pathological examination. Results The hind paw volume, serum (except VEGF) and synovial tissue in model group were significantly higher than those in normal group, and the expression of p-ERK1 / 2 in synovium was also increased (P <0.05 or P <0.01) ), Pathological section showed a large number of inflammatory cell infiltration, joint cartilage and joint surface serious damage, erosion of bone substance, structural disorders. However, the levels of IL-1β, TNF-α and Ang-1 in compound triptolide group were decreased, while the levels of cytokines and mRNA were decreased and the expression of p-ERK1 / 2 was decreased in synovial tissue (P <0.05 or P < 0.01). Pathology showed that compound Tripterygium topical has a good effect of inhibiting synovial tissue proliferation, reducing infiltration of inflammatory cells, and retarding the destruction of bone and cartilage. Conclusion Compound Tripterygium topicalis may reduce the synovial tissue proliferation, decrease the synovial angiogenesis and angiogenesis by decreasing the levels of inflammatory cytokines in synovial tissue of arthritis and attenuating the activation of ERK pathway.