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目的探讨奥芬米洛对实验性自身免疫性脑脊髓炎(EAE)大鼠发病的预防作用及其机制。方法 40只大鼠随机分为正常对照组、模型对照组、环孢素(10 mg·k~(-1))组和奥芬米洛(1.0 mg·kg~(-1))组,每组10只。除正常对照组大鼠外,其余各组大鼠双后脚掌皮下注射豚鼠全脊髓匀浆-完全福氏佐剂(GPSCH-CFA)0.4 mL进行免疫,同时奥芬米洛组和环孢素组经口灌胃给予相应的药物,每日1次,连续给药18 d。观察各组大鼠体重、神经功能评分、MBP抗体、Th1细胞因子(IFN-γ、TNF-α和IL-2)和Bcl-2/Bax蛋白表达的变化。结果奥芬米洛组EAE大鼠无临床症状发生;与模型对照组比较,奥芬米洛组大鼠血清中MBP抗体、IFN-γ、TNF-α和IL-2水平均明显降低(P<0.05或P<0.01),大脑皮质和下丘脑Bcl-2蛋白表达均明显升高(P<0.05或P<0.01),大脑皮质Bax蛋白表达明显降低(P<0.05)。结论奥芬米洛能抑制EAE大鼠的发病,其作用机制可能与抑制Th1细胞活性有关。
Objective To investigate the preventive effect and mechanism of Orphenamine on the pathogenesis of experimental autoimmune encephalomyelitis (EAE) in rats. Methods Forty rats were randomly divided into normal control group, model control group, cyclosporine (10 mg · k ~ (-1)) group and offenamil (1.0 mg · kg ~ (-1) Group of 10. Except rats in normal control group, all the rats in other groups were immunized with 0.4 mL of whole spinal cord homogenate - complete Freund’s adjuvant (GPSCH-CFA) Oral gavage given the appropriate drug, once daily, continuous administration of 18 d. The changes of body weight, neurological function score, MBP antibody, Th1 cytokines (IFN-γ, TNF-αand IL-2) and Bcl-2 / Bax protein expression in each group were observed. Results There was no clinical symptom in the rats of the OVA group. Compared with the model control group, serum levels of MBP antibody, IFN-γ, TNF-α and IL-2 in the OVA group were significantly decreased (P < 0.05 or P <0.01). The expression of Bcl-2 protein in cerebral cortex and hypothalamus were significantly increased (P <0.05 or P <0.01), and the expression of Bax protein in cerebral cortex decreased significantly (P <0.05). Conclusion Offenium can inhibit the pathogenesis of EAE rats and its mechanism may be related to the inhibition of Th1 cell activity.