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目的观察瘫痿胶囊对实验性自身免疫性重症肌无力(EAMG)的作用机制。方法以乙酰胆碱受体α1肽(AChRα1肽)多点注射法制备EAMG模型小鼠,将造模成功的58只健康雌性C57BL/6小鼠随机分为7组:模型组,瘫痿胶囊低、中、高剂量组,强的松组及正常组、佐剂组,观察其症状变化,检测其血清乙酰胆碱受体抗体(AChR-Ab)、转化生长因子β1(TGF-β1)、白介素4(IL-4)水平。结果4周后,与模型组比较,瘫痿胶囊高中剂量组及强的松组临床症状评分减少(P<0.01),AChR-Ab降低(P<0.01),TGF-β1升高(P<0.05),IL-4降低(P<0.05)。结论瘫痿胶囊治疗EAMG的机制可能是通过升高外周血TGF-β1水平、降低IL-4,抑制AChR-Ab的产生,从而改善临床症状。
Objective To observe the mechanism of Fuling Capsule on experimental autoimmune myasthenia gravis (EAMG). Methods EAMG model mice were prepared by multiple injections of acetylcholine receptor alpha 1 peptide (AChRα1 peptide). 58 healthy female C57BL/6 mice were randomly divided into 7 groups: model group, low and middle capsules. High-dose group, prednisone group, normal group, and adjuvant group were used to observe the changes of symptoms and detect serum acetylcholine receptor antibody (AChR-Ab), transforming growth factor β1 (TGF-β1), and interleukin 4 (IL- 4) Level. Results After 4 weeks, compared with the model group, the scores of clinical symptoms in the high-dose group and the prednisone group decreased (P<0.01), AChR-Ab decreased (P<0.01), and TGF-β1 increased (P<0.05). ), IL-4 decreased (P < 0.05). Conclusion The mechanism of EAMG in treating EAMG may be to improve clinical symptoms by increasing the level of TGF-β1 in peripheral blood, decreasing IL-4 and inhibiting the production of AChR-Ab.