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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IL-4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。
Objective To investigate the immunoregulatory mechanism of atorvastatin in experimental autoimmune myasthenia gravis (EAMG) rats. Methods The myasthenia gravis (MG) model of Lewis rats was immunized with artificial subunit α-subunit 97-116 of rat acetylcholine receptor and then randomly divided into atorvastatin treatment group and control group. Lennon scale The condition of rats was evaluated by double-blind method. The muscle mass of rats was assessed by double-blind method and the body weight was recorded. Immunohistochemistry was used to detect the expression of Foxp3, a thymus regulator, to reflect the number of regulatory T cells (Tregs) 8 to detect lymphonuclear mononuclear cell proliferation; ELISA detection of cell culture supernatant IL-4 and serum anti-R97-116 antibody levels. Results Compared with the control group, the clinical symptoms of atorvastatin group were significantly relieved. The expression of Foxp3 in thymus and the level of IL-4 in cell culture supernatant were higher than those in control group. The serum anti-R97-116 antibody level was lower than that in control group. Conclusions Atorvastatin can reduce the serum levels of anti-R97-116 antibody and alleviate the EAMG condition by up-regulating the levels of Treg and Th2 cytokine IL-4.