首页> 中文期刊> 《海南医科大学学报(英文版)》 >Study on anti-inflammatory mechanism and effects of Flemingia Roxb.exAit extract intervene acute gouty arthritis in rats

Study on anti-inflammatory mechanism and effects of Flemingia Roxb.exAit extract intervene acute gouty arthritis in rats

         

摘要

Objective:To investigate the effect and anti-inflammatory mechanism the effect of Flemingia Roxb.exAit extract on acute gouty arthritis.Methods:Sixty SD rats were randomly divided into 6 groups by weight,control and model group,(100、150、200 mg/kg)of Flemingia Roxb.exAit extract group and colchicine group.The rats of each group were given by intragastric for 7 days of continuous administration,meanwhile,there were given 0.9%NaCl solution instead as control and model group.The acute gouty arthritis model was constructed through right ankle joint cavity injection of sodium urate crystal solutionon day 5 after 1 h,but rats in the negative control group were injected with 0.9%NaCl solution into the articular cavity of the right foot.The general condition of rats and the degree of joint swelling,and the gait was observed after constructed model.To detected the joint fluid IL-1β、TNF-α、IL-6 indicators,and the expression of NLRP3,Caspase-1 protein in ankle joint tissue for 2 hours after the last administration.Results:Groups of Flemingia Roxb.exAit extract could markedly reduce the joint swelling on acute gouty arthritis rat model,improve gait in a dose-dependent manner,high dose group of Flemingia Roxb.exAit extract did particularly well(Pjoint swelling<0.01;Pgait<0.05),close to the therapeutic effect colchicine group.Further mechanism studies show that the joint fluid IL-1β、TNF-α、IL-6 level was reduced by Flemingia Roxb.exAit extract group,the expressions of NLRP3、Caspase-1 protein of Flemingia Roxb.exAit extract group was decreased observbly than model group,but the most obvious is that high dose group as well as colchicine group(PNALP3<0.01;PCaspase-1<0.01).Conclusion:Flemingia Roxb.exAit extract has the effect of treating acute gouty arthritis and its mechanism may be related toinhibiting NLRP3 inflammasome activation and inhibiting inflammatory response.

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