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背景:研究发现,肿瘤坏死因子(tumornecrosisfactor-alfa,TNF-α)在急性实验性变应性脑脊髓炎(experimentalallergicencephalomyelitis,EAE)的发病机制中起着重要作用,它可以介导少突胶质细胞的凋亡及脱髓鞘,是EAE脑内重要的炎性细胞因子之一。目的:探索EAE豚鼠脑白质TNF-αmRNA的表达以及己酮可可碱、培高利特对其表达的影响。设计:随机对照实验。地点和对象:研究在重庆医科大学附属第一医院神经病学研究所完成,重庆医科大学动物实验中心提供的成年、体质量200～350g豚鼠为研究对象。方法:采用免疫诱导方法制备EAE豚鼠模型,应用RT-PCR方法检测EAE豚鼠脑白质TNF-αmRNA的表达。主要观察指标:①成功制模。②TNF-αmRNA表达的半定量分析。结果:EAE组豚鼠脑白质TNF-αmRNA的表达(1.11±0.06)明显高于对照组(0.32±0.02)(P<0.01),治疗组(0.51±0.03,0.76±0.03)较EAE组表达下降(P<0.05)。结论:急性EAE豚鼠脑白质TNF-αmRNA的表达上调,与疾病的触发有关,己酮可可碱、培高利特对TNF-αmRNA的表达具有不同程度的抑制作用。
BACKGROUND: The study found that tumor necrosis factor-α (TNF-α) plays an important role in the pathogenesis of experimental experimental allergic encephalomyelitis (EAE). It can mediate oligodendrocyte Apoptosis and demyelination, is one of the important inflammatory cytokines in EAE brain. Objective: To explore the expression of TNF-αmRNA and the effects of pentoxifylline and pergolide on EAE guinea pig white matter. Design: Randomized controlled experiment. Location and Subjects: The study was completed at the Institute of Neurology, the First Affiliated Hospital of Chongqing Medical University, and adult guinea pigs weighing 200-350 g provided by the Animal Experimental Center of Chongqing Medical University were studied. Methods: EAE guinea pig model was induced by immune induction. The expression of TNF-αmRNA in white matter of EAE guinea pigs was detected by RT-PCR. MAIN OUTCOME MEASURES: ① successful model. ② Semi-quantitative analysis of TNF-α mRNA expression. Results: The expression of TNF-αmRNA in EAE group was significantly higher than that in EAE group (1.11 ± 0.06 vs 0.32 ± 0.02, P <0.01) P <0.05). CONCLUSION: The up-regulation of TNF-αmRNA in white matter of EAE rats is related to the triggering of the disease. Pentoxifylline and pergolide can inhibit the expression of TNF-αmRNA to some extent.