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目的探讨实验性变态反应性脑脊髓炎模型(EAE)脑组织细胞因子的变化,探讨阿托伐他汀对EAE发病保护作用的免疫调节机制。方法皮下注射粗制碱性髓鞘蛋白(MBP)建立EAE模型。用40只豚鼠分成4组:正常对照组、EAE对照组、EAE小剂量组和EAE大剂量组,每组10只,雌雄各半,用放射免疫法测定正常对照组、EAE各组高峰期脑组织细胞因子白细胞介素-1β(IL-1β)、肿瘤坏死因子α(TNF-α)含量。结果EAE对照组、EAE小剂量组和EAE大剂量组脑组织细胞因子IL-1β水平分别为2.85±0.70、1.97±0.44、1.57±0.45 ng/mg,显著高于正常对照组0.51±0.02 ng/mg,EAE大、小剂量组脑组织IL-1β水平比EAE对照组低,EAE大剂量组脑组织IL-1β水平比EAE小剂量组低(P<0.05);EAE对照组、EAE小剂量组和EAE大剂量组脑组织细胞因子TNF-α水平分别为2.83±0.90、1.98±0.44、1.46±0.35 ng/mg,显著高于正常对照组水平(1.13±0.28 ng/mg),EAE大、小剂量组脑组织TNF-α水平比EAE对照组低;EAE大剂量组TNF-α水平比EAE低剂量组低(P<0.05)。结论EAE豚鼠存在明显免疫功能紊乱,阿托伐他汀有降低EAE模型脑组织IL-1β、TNF-α水平作用,其对EAE发病的免疫保护机制可能是通过抑制IL-1β、TNF-α产生而发挥。
Objective To investigate the changes of cytokines in experimental allergic encephalomyelitis model (EAE) and to explore the immunoregulatory mechanism of atorvastatin on the pathogenesis of EAE. Methods EAE model was established by subcutaneous injection of crude basic myelin protein (MBP). 40 guinea pigs were divided into 4 groups: normal control group, EAE control group, EAE low-dose group and EAE high-dose group, 10 in each group, male and female, radioimmunoassay normal control group, EAE peak brain The levels of cytokines interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) were measured. Results The levels of IL-1β in brain tissue of EAE control group, EAE low-dose group and EAE high-dose group were 2.85 ± 0.70, 1.97 ± 0.44 and 1.57 ± 0.45 ng / mg, respectively, which were significantly higher than those of the control group 0.51 ± 0.02 ng / (P <0.05). EAE control group, EAE low dose group (P <0.05), EAE control group, EAE low dose group And EAE high dose group were 2.83 ± 0.90, 1.98 ± 0.44 and 1.46 ± 0.35 ng / mg, respectively, which were significantly higher than those of the normal control group (1.13 ± 0.28 ng / mg) Compared with EAE control group, TNF-αlevel of EAE high dose group was lower than EAE low dose group (P <0.05). Conclusions EAE guinea pigs have obvious immune dysfunction. Atorvastatin can reduce the levels of IL-1β and TNF-α in EAE model rats. The protective mechanism of EA on EAE may be through inhibiting the production of IL-1β and TNF-α Play