祛湿除痹中药对急性痛风性关节炎模型大鼠的抗炎机制研究

【目的】通过观察祛湿除痹中药对急性痛风性关节炎模型大鼠踝关节内急性炎症反应通道的影响,探讨其对急性痛风性关节炎模型的抗炎作用机制。【方法】复制急性痛风性关节炎模型,将40只Wistar大鼠随机分为5组(每组8只):空白对照组、模型对照组、秋水仙碱组(剂量为9 mg.kg-1.d-1)、中药高剂量组(剂量为54 g.kg-1.d-1)、中药低剂量组(剂量为27 g.kg-1.d-1)。连续灌药7 d后取材,观察各组对大鼠关节肿胀度及关节内炎症细胞、炎症因子白细胞介素及其受体(IL-1β、IL-1R)及髓样细胞分化因子(MyD88)表达的影响。【结果】各给药组炎症细胞计数、IL-1β、IL-1R、MyD88表达水平显著低于模型对照组(均P<0.05或P<0.01),其中中药高剂量组各炎症指标表达水平显著低于秋水仙碱组(均P<0.05),中药低剂量组各炎症指标与秋水仙碱组比较差异无统计学意义(P>0.05)。【结论】祛湿除痹中药可通过阻断IL-1R-MyD88信号通路而减轻急性痛风性关节炎模型大鼠踝关节内炎症反应。

Anti-inflammatory Mechanism of Dampness-dispelling and Obstruction-removing Herbal Medicine for Treatment of Acute Gouty Arthritis Model Rats

Objective To observe the effect of dampness-dispelling and obstruction-removing herbal medicine on inflammatory signaling pathway in model rat ankles with acute gouty arthritis,and to explore its anti-inflammatory mechanism.Methods Forty Wistar rats were equally randomized into 5 groups,blank control group,model group,colchicine(9 mg·kg-1·d-1) group,and high-dose(54 g·kg-1·d-1)and low-dose(27 g·kg-1·d-1)herbal medicine groups.Rat model of acute gouty arthritis were established,and rats in the medication groups were given gastric gavage of corresponding drugs according to the experimental design.After treatment for 7 days,the metatarsal swelling,inflammatory cell count,and the expression of inflammatory cytokines of interleukin and its receptor(IL-1β and IL-1R)as well as the myeloid differentiation factor 88(MyD88)were observed.Results The three medication groups had lower inflammatory cell count and lower expression levels of IL-1β,IL-1R and MyD88 than the model group(P<0.05 or P<0.01).High-dose herbal medicine group had lower expression levels of inflammatory indicators than colchicine group(P<0.05),but the differences of expression levels of inflammatory indicators were insignificant between low-dose herbal medicine group and colchicine group(P>0.05).Conclusion Dampness-dispelling and obstruction-removing herbal medicine can relieve the inflammatory reaction in rat ankles with acute gouty arthritis by blocking the inflammatory IL-1R-MyD88 signaling pathway.