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目的:研究选择性白介素(IL)-6抑制剂Am-80对实验性自身免疫性脑炎(EAE)的影响,并分析IL-6在EAE发病过程中的作用.方法:诱导大鼠EAE模型.半定量RT-PCR检测大鼠脊髓中细胞因子mRNA表达,培养RAW264.7细胞测定一氧化氮(NO).结果:Am-80(1.0,3.0 mg/kg,ig×12 d)能抑制髓鞘质缄性蛋白引起的DA大鼠EAE症状,但高剂量Am-80并不能完全抑制EAE发病,而只能延缓EAE发作时间,停止给药后EAE病症仍然出现并有症状增强的现象;延长Am-80的给药时间(18 d),EAE仍然会在停止用药后出现.RT-PCR证明12 d Am-80给药能抑制EAE大鼠脊髓中IFN-γ,IL-6,IL-10,TGF-β1.TNF-α和iNOS的mRNA表达水平,但停药后一天(d 13)其它因子没有变化而IL-6 mRNA水平上升;进一步采用DA大鼠EAE模型证明:分别给予12 d和18 d Am-80后,IL-6 mRNA表达水平的上升出现在停药后一天的EAE大鼠脊髓中.结论:IL-6可能是EAE发病过程中的一个关键因素.
Objective: To investigate the effect of interleukin-6 (IL-6) inhibitor Am-80 on experimental autoimmune encephalitis (EAE) and to analyze the role of IL-6 in the pathogenesis of EAE.Methods: .The mRNA expression of cytokines in rat spinal cord was detected by semi-quantitative RT-PCR, and the level of nitric oxide (NO) in RAW264.7 cells was detected.Results Am-80 (1.0, 3.0 mg / kg, ig × 12 d) However, the high dose of Am-80 did not completely inhibit the onset of EAE, but delayed the attack time of EAE. After EAE, EAE still appeared and the symptoms increased. The administration of Am-80 for 18 d, EAE still appears after stopping the medication.RT-PCR proved that 12 d Am-80 administration can inhibit EAE rat spinal cord IFN-γ, IL-6, IL-10 , TGF-β1.TNF-α and iNOS mRNA expression levels, but one day after drug withdrawal (d 13), other factors did not change and IL-6 mRNA levels increased; further use of DA rats EAE model proved: were given 12 d and After 18 d Am-80, the expression of IL-6 mRNA increased in the spinal cord of EAE rats one day after withdrawal.Conclusion: IL-6 may be a key factor in the pathogenesis of EAE.