首页> 中文期刊> 《中国结合医学杂志:英文版》 >Therapeutic Mechanism of Santeng Dingtong Recipe (三藤定痛方) on Monosodium Urate Crystal-Induced Rabbit Arthritis

Therapeutic Mechanism of Santeng Dingtong Recipe (三藤定痛方) on Monosodium Urate Crystal-Induced Rabbit Arthritis

         

摘要

Objective: To study the therapeutic mechanism of Santeng Dingtong recipe (STDT) on monosodium urate crystal (MSU) induced rabbit arthritis. Methods: Forty-two rabbits were randomly divided into six groups, 7 in each group. Group 1 收稿 0.9% saline 2.5 ml/kg per day by gastrogavage (ig) for 10 days; Group 2, 3 and 4 收稿 STDT 0.125 g/kg, 1.0 g/kg and 8.0 g/kg per day respectively by ig for 10 days; Group 5 收稿 colchicine 4.5 mg/kg per day by ig for 4 days; and Group 6 was untreated. MSU crystals 10 mg /500 μl containing polymyxin B 10 u/ml was injected into the knee joints of Group 1-5 to make rabbit arthritis models. Leukocytes in synovial lavage fluids was then counted and differentiated; pathological injury of synovial membranes was observed under HE staining; interleukin-1 beta (IL-1β), tumor necrosis factor alpha (TNFα) and leukotriene B4 (LTB4) content in synovial lavage fluids were determined by ELISA. Results: MSU caused a rapid leukocyte infiltration and increased production of IL-1β, TNFα and LTB4 2 hrs after intra-articular injection. STDT inhibited neutrophil infiltration in synovial fluids dose-dependently, protected the synovial membrane against pathological injury and reduced the production of IL-1β, TNFα and LTB4; while colchicine did not decrease the level of TNFα, but significantly inhibited neutrophil infiltration in synovial fluid and reduced the production of IL-11β and LTB4. Conclusion: STDT exerts an anti-inflammatory effect in rabbit model of acute MSU arthritis, its mechanism being probably due to the decrease of IL-1β, TNFα and LTB4 synthesis.

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