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目的探讨益肾Ⅰ方治疗佐剂性关节炎的药理作用及其作用机制。方法制备佐剂性关节炎大鼠模型,观察益肾Ⅰ方对病鼠超敏反应性炎症左、右后足跖厚度以及病鼠血清肿瘤坏死因子(TNF)-α,循环免疫复合物(CIC),丙二醛(MDA)含量和超氧化物歧化酶(SOD)活性的影响:结果益肾Ⅰ方能抑制佐剂性关节炎大鼠继发性、自身免疫性足跖肿胀,疗效随疗程延长而效果愈为明显,差异有高度显著陛(P<0.01);降低病鼠增高的TNF-α,CIC,MDA含量,提高其低下的SOD活性,差异均有高度显著性(P<0.01):结论益肾Ⅰ方具有对抗大鼠佐剂性、继发性关节炎的作用,其机制与抑制自由基损伤和降低自身免疫的病理生理性反应有关。
Objective To investigate the pharmacological effects of Yishen I prescription on adjuvant arthritis and its mechanism of action. METHODS: A rat model of adjuvant arthritis was prepared to observe the thickness of left and right hind paws of hypersensitivity inflammation in mice, serum tumor necrosis factor (TNF)-α, and circulating immune complexes (CIC) in rats. ) Effects of malondialdehyde (MDA) content and superoxide dismutase (SOD) activity: Results Yiyi I can inhibit the secondary, autoimmune paw edema in adjuvant arthritis rats, and the curative effect is related to the course of treatment. The effect was prolonged, the more obvious the effect was, the difference was highly significant (P<0.01); the increase of TNF-α, CIC, MDA content in the diseased mice, and the increase of its low SOD activity were highly significant (P<0.01). :Conclusion Yishen I has anti-addiction and secondary arthritis effects in rats, and its mechanism is related to inhibition of free radical damage and reduction of autoimmune pathophysiological responses.