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目的:观察新痹痛灵对胶原诱导性关节炎大鼠及其滑膜组织中HMGB1 mRNA的影响。方法:新痹痛灵方中饮片经相关工艺提取后制为浸膏;将SD大鼠72只随机分出12只为正常组,其余进行胶原诱导性关节炎(CIA)造模,再将造模大鼠随机分为模型组,新痹痛灵高、中、低剂量组(3.2,1.6,0.8 g·kg-1·d-1)以及雷公藤多苷片组(0.008 g·kg-1·d-1),各组大鼠于二次免疫后当天开始ig给药,连续给药21 d。容积法测量大鼠关节体积,病理切片观察,RT-q PCR检测滑膜组织HMGB1mRNA的表达。结果:与正常组比较,模型组大鼠关节肿胀明显(P<0.01),滑膜组织HMGB1 mRNA的表达明显增加(P<0.01);与模型组比较,新痹痛灵高剂量组的关节肿胀于14,21 d明显减轻(P<0.05,P<0.01),且滑膜组织HMGB1 mRNA的表达明显降低(P<0.01)。关节病理切片显示新痹痛灵各剂量组及雷公藤多苷片组病变较模型组均有不同程度减轻。结论:新痹痛灵可减轻CIA大鼠关节肿胀、降低滑膜组织中HMGB1 mRNA的表达,通过抑制HMGB1而减少相关炎症通路的激活可能是新痹痛灵治疗类风湿关节炎的机制之一。
Objective: To observe the effects of xipongling on HMGB1 mRNA in collagen-induced arthritis rats and its synovial tissue. Methods: Xintonglingfangzhong decoction was extracted by the relevant technology and then extracted into the extract. Seventy-two SD rats were randomly divided into normal group and 12 rats in the control group. Collagen-induced arthritis (CIA) The rats were randomly divided into model group, high, medium and low doses of Bitongling (3.2,1.6,0.8 g · kg-1 · d-1) and Tripterygium wilfordii tablet group (0.008 g · kg-1 · D-1), the rats in each group began ig administration on the day after the second immunization, and were administered continuously for 21 days. Volumetric method was used to measure the joint volume of rats. The pathological sections were observed. The expression of HMGB1 mRNA in synovial tissue was detected by RT-q PCR. Results: Compared with the normal group, the joint swelling in the model group was significantly (P <0.01) and the expression of HMGB1 mRNA in the synovium was significantly increased (P <0.01). Compared with the model group, (P <0.05, P <0.01), and the expression of HMGB1 mRNA in synovium significantly decreased (P <0.01). Arthroscopic pathological sections show that the new Bitong Ling dose groups and Tripterygium tablets group lesions than the model group were reduced to varying degrees. CONCLUSIONS: New Bitongling can reduce the swelling of joints and decrease the expression of HMGB1 mRNA in synovium of CIA rats. It may be one of the mechanisms for the treatment of rheumatoid arthritis by the new Bitongling by inhibiting the activation of HMGB1.