中文摘要：

摘要：目的探究阿托伐他汀对实验性自身免疫性重症肌无力（EAMG）大鼠的免疫调节机制。方法用人工合成的大鼠乙酰胆碱受体α亚基97-116肽段免疫Lewis大鼠制造重症肌无力（MG）模型，随机分为阿托伐他汀治疗组和对照组，采用Lennon评分标准评价大鼠病情，采用双盲法隔天评估大鼠肌力并记录体质量；免疫组化检测大鼠胸腺抑制性转录调节因子Foxp3的表达，以此反映调节性T细胞（Treg）的数量；CCK-8检测淋巴结单个核细胞增殖；ELISA检测细胞培养上清液IL4及血清抗R97-116抗体的水平。结果阿托伐他汀治疗组大鼠临床症状较对照组明显缓解，胸腺Foxp3的表达及细胞培养上清液IL-4的水平均高于对照组，血清抗R97-116抗体水平低于对照组。结论阿托伐他汀通过上调Treg和Th2型细胞因子IL-4的水平，从而降低血清中抗R97-116抗体水平，缓解EAMG病情。

英文摘要：

Objective To investigate the immunological mechanism of atorvastatin in experimental autoimmune myas- thenia gravis （EAMG） in rats. Methods Atorvastatin was administered intraperitoneally to the EAMG rats. The intra- thymic expression of fork head box protein 3 （ Foxp3 ） was analyzed by the immunohistochemistry and the lymphocyte proliferation was determined by CCK-8. The level of IL-4 in culture supernatants of lymph node mononuclear cells （MNC） and anti-R97-116 IgG in the serum were detected by ELISA. Results Administration of atorvastatin ameliora- ted clinical signs of EAMG, increased the number of the Foxp3-positive cells in the thymic medulla, up regulated the level of IL-4 in culture supematants, and decreased the level of serum anti-R97-116 IgG. Conclusion Lower dose of atorvastatin could ameliorate EAMG by up-regulation of Treg and Th2 cytokines.