上中下通用痛风汤治疗急性痛风性关节炎及对Th17细胞的影响

Effect of Shangzhongxia General Gout Decoction on Acute Gouty Arthritis and Th17 Cells

摘要:

目的：研究上中下通用痛风汤对尿酸钠诱导大鼠急性痛风性关节炎（GA）的治疗作用及对Th17细胞的影响。方法：取 60 只大鼠，随机分成 6 组，对照组、模型组、吲哚美辛组、上中下通用痛风汤高、中、低剂量组（20，10，5 g·kg^-1），每组 10 只。上中下通用痛风汤组ig给药，1次/d，连续7 d，吲哚美辛（5 mg·kg^-1）组第7天开始给药，末次给药1 h后，按Coderre经典方法，除空白组外，其余5 组采用尿酸钠晶体溶液踝关节注射建立急性痛风性关节炎模型。以上中下通用痛风汤与吲哚美辛对比治疗，观察大鼠步态，测定关节肿胀度，流式细胞术检测外周血Th17细胞含量，ELISA方法检测血清白介素（IL）-17，IL-6水平。结果：上中下通用痛风汤高、中、低剂量在致炎后各时间点均能不同程度的抑制尿酸钠所致大鼠踝关节疼痛，减轻肿胀程度，降低步态评分，降低外周血Th17细胞含量。高剂量组Th17细胞含量（1.65±0.25）%明显低于模型组（3.25±0.96）%，相关炎性因子IL-17含量（0.54±0.09）μg·L^-1明显低于模型组（0.69±0.07）μg·L^-1，IL-6含量亦明显低于模型组，差异有显著性（P<0.05）。结论：上中下通用痛风汤对尿酸钠所致急性痛风性关节炎症有较好的抗炎镇痛作用，其作用机制可能与降低Th17细胞及炎症因子IL-17，IL-6水平有关。

Abstract:

Objective: To study anti-inflammatory and analgesic effects of Shangzhongxia generic gout decoction (SGGD) on sodium urate induced acute gouty arthritis (GA). Method: 60 rats were randomly divided into six groups, the control group, the model group, indomethacin group, SGGD high dose group, middle dose group, low dose group (20, 10, 5 g·kg^-1), 10 in each group. SGGD was given once each day for 7 days.1 h after the last administration, according to the classical method Coderre, in addition to the control group, and rats in the remaining five groups were injected ankle injection of sodium urate crystal solution to establish acute gouty arthritis model. The degree of joint swelling were measured the, Flow cytometry was used to detect the content of peripheral blood Th17 cells, ELISA was used to detect serum IL-17, IL-6. Result: SGGD inhibited sodium urate induced ankle pain, decreased the levels of Th17 in peripheral blood, in high dose group, Th17 cells (1.65±0.25) % was significantly lower than that in the model group (3.25±0.96) %. Th17 cell related inflammatory factor IL-17 (0.54±0.09) μg·L^-1 was significantly lower than that in the model group (0.69±0.07) μg·L^-1. Inflammatory IL-6 content was obviously lower than that in the model group (P<0.05). Conclusion: SGGD has better therapeutic effect on sodium urate gouty arthritis, the mechanism may be related to the decreasing Th17 cells and the level of inflammatory factors IL-17, IL-6.