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目的观察阿托伐他汀对实验性自身免疫性脑脊髓炎(EAE)的治疗作用并初步探讨其治疗机制。方法将大鼠分为正常组、模型组、阿托伐他汀组,每组6只。正常组不做任何处理;以豚鼠脑、脊髓为原料提取髓鞘碱性蛋白(MBP),免疫Lewis大鼠建立EAE模型。模型组注射抗原后以蒸馏水灌胃,阿托伐他汀组给予阿托伐他汀灌胃。建模后每日对大鼠神经症状进行评分,采用MTT法检测T淋巴细胞增殖,ELISA法检测大鼠脾细胞培养上清液中IFN-γ和IL-4水平。结果 (1)与模型组相比,阿托伐他汀组大鼠神经系统症状有不同程度减轻;(2)MTT法显示:与模型组大鼠相比,阿托伐他汀组大鼠的T细胞增殖被显著抑制(P<0.01);(3)与正常组相比,模型组大鼠13d时IL-4水平无明显变化,17、21d时,IL-4水平明显升高(P<0.01),与模型组相比,阿托伐他汀组13、17d时IL-4水平明显升高(P<0.01),IFN-γ水平在13、17、21d时均显著低于模型组(P<0.05)。结论阿托伐他汀能改善EAE大鼠的症状,其机制可能与抑制T淋巴细胞增殖,纠正Th1/Th2失衡有关。
Objective To observe the therapeutic effect of atorvastatin on experimental autoimmune encephalomyelitis (EAE) and to explore its therapeutic mechanism. Methods The rats were divided into normal group, model group and atorvastatin group, with 6 rats in each group. The normal group was treated with no treatment. The myelin basic protein (MBP) was extracted from the brain and spinal cord of guinea pigs and Lewis rats were immunized to establish EAE model. The model group was injected with distilled water after intragastric administration of antigen, and atorvastatin group was given intragastric administration of atorvastatin. After modeling, the neurological symptoms of rats were scored daily. The proliferation of T lymphocytes was detected by MTT assay. The levels of IFN-γ and IL-4 in the culture supernatant of splenocytes were detected by ELISA. Results (1) Compared with the model group, the neurological symptoms of atorvastatin group were alleviated to some extent. (2) Compared with the model group, the T cells in atorvastatin group (3) Compared with the normal group, the level of IL-4 in the model group did not change significantly on the 13th day and the level of IL-4 on the 21st and 21st day was significantly increased (P <0.01) Compared with the model group, the level of IL-4 in atorvastatin group was significantly increased at 13 and 17 days (P <0.01), while the level of IFN-γ at 13 and 17 and 21 days in model group was significantly lower than that in model group ). Conclusions Atorvastatin can improve the symptoms of EAE rats. The mechanism may be related to the inhibition of T lymphocyte proliferation and the correction of the imbalance of Th1 / Th2.