鬼针草总黄酮对大鼠佐剂性关节炎的治疗作用及机制

目的 探讨鬼针草总黄酮(TFB)对大鼠佐剂性关节炎(AA)关节肿胀指数、炎症因子水平、toll样受体4（TLR4）信号转导通路及病理评分的影响。方法 选取50只雄性SD大鼠，随机分为空白组、模型组、TFB(40 mg/kg、80 mg/kg、160 mg/kg)组，每组各10只。比较各组大鼠关节肿胀指数；采用放射免疫法检测血清白细胞介素1β（IL-1β）、肿瘤坏死因子α（TNF-α）的水平；Western blotting检测巨噬细胞中TLR4、核因子κB（NF-κB）的表达水平；HE染色进行大鼠关节病理评分。结果 模型组关节肿胀指数、炎症因子水平、TLR4及NF-κB表达均明显高于空白组，不同剂量的TFB组（40 mg/kg、80 mg/kg、160 mg/kg）关节肿胀指数、炎症因子水平、TLR4、NF-κB表达及病理评分均显著低于模型组(P<0.05)，且TFB剂量越大，所有指标表达水平越低(P<0.05)。结论 TFB对AA大鼠具有治疗作用，其作用机制可能与降低关节肿胀指数及炎症因子水平、抑制TLR4和NF-κB表达、阻碍血管翳形成有关。

Treatment and mechanism in total flavonoids of Bidens on adjuvant arthritis in rats

Objective To investigate the effects of the total flavonoids of Bidens (TFB) on the joint swelling index, and the level of inflammatory factors, the toll-like receptor 4(TLR4) signal transduction pathway and the pathological score in the rats with adjuvant arthritis (AA). Methods Totally 50 male SD rats were randomly divided into blank group, model group, TFB (40 mg/kg, 80 mg/kg, 160 mg/kg) group, each group was 10. The swelling index of joint in each group was compared, and the level of serum interleukin-1β (IL-1β) and tumor necrosis factor α (TNF-α) was detected by radioimmunoassay. Western blotting was used to detect the expression of toll-like receptor 4(TLR4) and nuclear factor-kappa B (NF-κB) in macrophages, and HE staining was used to evaluate the pathological score of rat joints. Results The joint swelling index, the level of inflammatory factors, the expression of TLR4 and NF-κB in the model group were significantly higher than that in the blank group. In different doses of TFB group (40 mg/kg, 80 mg/kg; 160 mg/kg), the joint swelling index, inflammatory factor level, TLR4, NF-κB expression and pathological score were significantly lower than those in the model group (P<0.05), and the higher the dose of TFB, the lower the expression level of all the indexes. Conclusion TFB has therapeutic effects on AA rats, and its mechanism may be related to reducing the joint swelling index and inflammatory factor level, inhibiting the expression of TLR4 and NF-kappa B, and preventing pannus formation.