摘要
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 explore the mechanism of Tanwei Capsule （Capsule for paralysis） on the experimental autoimmune myasthenia gravis （EAMG）. Methods The EAMG mice model were made with AChRα1 injection. The 58 healthy female C57BL/6 mice models were randomized into 7 groups： model group, Tanwei Capsule tow, medium and high dosage groups, prednisone group, normal group, and adjuvant group. Symptoms, serum acetylchoiine receptor antibody （AchR-Ab）, transforming growth factor-β1 （TGF-β1） and Interleukin-4（IL-4） were observed. Results Four weeks later, compared with the model group, the scores of Tanwei Capsule high and medium dosage groups and prednisone group were decreased （P〈0.01）, AchR-Ab decreased （P〈0. 01）, TGF-β1 increased （P〈0.05）, and IL-4 decreased （P〈0.05）. Conclusion The mechanism of Tanwei Capsule relieving clinical symptoms of EAMG is possibly through increasing TGF-β1, decreasing IL-4, and inhibiting the production of AehR-Ab.
出处
《中医杂志》
CSCD
北大核心
2008年第11期1028-1030,共3页
Journal of Traditional Chinese Medicine
关键词
实验性自身免疫性重症肌无力
瘫痿胶囊
乙酰胆碱受体抗体
神经重复电刺激
白细胞介素4
转化生长因子Β1
Experimental autoimmune myasthenia gravis （EAMG）
Tanwei Capsule （Capsule for paralysis）~ Acetylcholine receptorantibody （AchR-Ab）
Interleukin-4（IL-4）
Transgrowth factor-β1（TGF-β1）
