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目的:观察豨桐丸对尿酸钠晶体诱导的大鼠痛风性关节炎的影响及其药理机制。方法:分别给予大鼠豨桐丸(200,400,800 mg·kg-1)及秋水仙碱(4 mg·kg-1)灌胃用药7 d。第5天大鼠踝关节腔注射尿酸钠晶体诱导痛风性关节炎模型。检测大鼠足肿胀和步态评分,苏木素-伊红(HE)染色法检测关节组织学评分,抗酒石酸酸性磷酸酶染色法检测破骨细胞形成,免疫组化法分析关节组织中肿瘤坏死因子(tumor necrosis factor,TNF)-α,白细胞介素(interleukin,IL)-1β和IL-6表达,蛋白免疫印迹法(Western blot)分析NLRP3炎性体表达。结果:注射尿酸钠晶体导致了大鼠明显的足肿胀,并使步态评分和组织学评分均明显增高,关节组织中的破骨细胞数量及TNF-α,IL-1β,IL-6和NLRP3炎性体表达也都明显增加((P<0.05,P<0.01)。给予400,800 mg·kg-1豨桐丸治疗后,大鼠足肿胀显著减轻,步态评分和组织学评分均显著减少,同时关节组织中的破骨细胞数量及TNF-α,IL-1β,IL-6和NLRP3炎性体表达也都显著降低(P<0.05,P<0.01)。结论:豨桐丸可抑制尿酸钠晶体诱导的大鼠痛风性关节炎的发展,其机制与抑制炎性介质的表达密切相关。
OBJECTIVE: To observe the effects and the pharmacological mechanisms of Davidiaotong pill on gouty arthritis induced by sodium urate in rats. Methods: The rats were administered with Radix Tong Pill (200,400,800 mg · kg -1) and colchicine (4 mg · kg -1) respectively for 7 days. Day 5 rat model of gouty arthritis induced by intrauterine injection of sodium urate. The foot swelling and gait scores of rats were measured. The joint histological scores were detected by hematoxylin and eosin (HE) staining and the formation of osteoclasts by tartrate-resistant acid phosphatase staining. The expression of tumor necrosis factor-α (TNF-α), interleukin (IL) -1β and IL-6, Western blot analysis was used to analyze the expression of NLRP3 inflammasome. RESULTS: Sodium percarbonate injections led to significant foot swelling in rats and significantly increased gait scores and histological scores. The number of osteoclasts and the levels of TNF-α, IL-1β, IL-6 and NLRP3 (P <0.05, P <0.01). After treatment with 400 and 800 mg · kg-1 of Tongtong Pill, the rats’ foot swelling was significantly reduced, the gait score and the histological score were significantly reduced, At the same time, the number of osteoclasts and the expressions of TNF-α, IL-1β, IL-6 and NLRP3 in articular tissues also decreased significantly (P0.05, P0.01) .Conclusion: Crystal-induced development of gouty arthritis in rats is closely related to the inhibition of the expression of inflammatory mediators.