青藤碱对大鼠佐剂性关节炎治疗作用及机制的研究

目的:观察青藤碱对佐剂性关节炎的治疗作用和对继发性炎症区域一氧化氮(NO)及相关炎症介质的影响,进一步探讨其治疗类风湿性关节炎的可能作用机制。方法:用Freund’s完全佐剂诱导大鼠佐剂性关节炎,设立正常组、模型组、泼尼松组、青藤碱低、中、高剂量组(30,60,120 mg.kg^-1),记录各组大鼠足跖肿胀度和关节炎指数,检测大鼠关节浸液内NO,前列腺素E₂(PGE₂)及细胞因子白细胞介素1(IL-1),肿瘤坏死因子(TNF)水平。结果:与正常组比较,模型组大鼠关节浸液内NO,PGE₂及IL-1,TNF水平显著升高(P<0.05);与模型组相比,青藤碱组大鼠佐剂性关节炎继发病变显著受抑制,佐剂性关节炎大鼠关节浸液内NO,PGE₂及细胞因子IL-1,TNF水平显著降低(P<0.05)。结论:青藤碱对类风湿性关节炎的治疗作用与其抑制炎症局部区域细胞因子活性和降低炎症介质含量有关,其中青藤碱使NO水平下降可能是抗类风湿性关节炎的重要作用机制。

Effect of sinomenine on adjuvant arthritis and its mechanisms

Objective: To discuss the anti-inflammatory mechanism of sinomenine on inflammatory media in joint of adjuvant arthritis rats. Method: Rats were randomly divided into the normal group and the model group, the prednisone group, the small, medium, large dosages of sinomenine group(30, 60, 120 mg·kg^-1). Except for the rats in the normal group, animals were modeled to adjuvant arthritis with freund's complete adjuvant. The arthritis index(AI) and the swelling degree of paws were recorded, and the activity of IL-1, TNF and the levels of NO, PGE₂ in joint fluids of secondary arthritis were determined. Result: Compared with the normal group, the activity of IL-1, TNF and the levels of NO, PGE₂ in joint fluids of secondary arthritis were increased significantly in the model group(P<0.05). Compared with the model group, it was shown to exert a dramatic inhibitory effect on secondary reaction of freund's adjuvant arthritis of rats, and the activity of IL1, TNF and the levels of NO, PGE₂ in joint fluids of secondary arthritis were significantly decreased in the sinomenine group(P<0.05). Conclusion: Sinomenine has a remarkable treatment effect on RA. It is via NO to inhibit the activity of cytokines and decrease the level of inflammation mediators, which may be one of its curing RA mechanism.