中文摘要：

目的 研究Nogo-A及其下游信号通路在MTLE患者颞叶皮层的表达，探讨其在癫痫后异常神经环路形成过程中的作用。 方法 收集本科MTLE患者颞叶皮层标本12例与正常颞叶皮层标本12例，采用RT-PCR、Western blot、免疫组化方法检测Nogo-A、NgR、P75（NTR）、Lingo-1、Troy表达情况。 结果 MTLE患者颞叶皮层致痫灶中出现神经元丢失、细胞排列结构紊乱、极性消失和胶质增生等病理改变。与正常对照相比，MTLE患者颞叶皮层Nogo-A mRNA和蛋白表达显著降低（P〈0.01），NgR mRNA和蛋白表达显著升高（P〈0.01）；Nogo-A蛋白在神经元中表达显著升高（P〈0.01），而在胶质细胞中表达显著降低（P〈0.01）；NgR、 P75（NTR）、Troy、Lingo-1蛋白主要表达于神经元中，其中前三者表达均显著升高（P〈0.05，P〈0.01），而Lingo-1蛋白表达降低不显著（P〉0.05）。 结论 Nogo-A及其下游信号通路在MTLE患者颞叶皮层中的表达发生改变，提示其非常可能参与了异常神经环路的形成过

英文摘要：

Objective To determine the expression of Nogo-A signaling pathway in the temporal lobe from mesial temporal lobe epilepsy （MTLE） patients and investigate its potential role in the formation of abnormal neural networks after epileptic seizure. Methods Twelve tissue samples of temporal lobe from diagnosed intractable MTLE patients during operation and 12 samples of normal temporal lobe due to traumatic wound debridement or tumor craniotomy were collected after informed consent signed and approval of the Ethics Committee of our hospital in our department from June 2011 to June 2012. The expression of Nogo-A, NgR, P75（NTR）, Lingo-1 and Troy was detected by RT-PCR, Western blotting and immunohistochemical assay. Results There were such pathological changes in the temporal lobe cortex from MTLE patients as neuron loss, disarranged order, neuron polarity loss, and gliosis. The expression of Nogo-A at mRNA and protein levels in MTLE patients was significantly down-regulated （P〈0.01）, while that of NgR was significantly up-regulated （P〈0.01） when normal individuals. The Nogo-A protein expression was significantly higher in the neurons （P〈0.01）, but significantly mild in glial cells （P〈0.01）. NgR, P75（NTR）, Troy and Lingo-1 proteins were mainly expressed in the neurons, which were significantly up-regulated （P〈0.05, P〈0.01） except Lingo-1 down-regulated though not significantly （P〉0.05）. Conclusion The expression of Nogo-A and its downstream signaling pathway is changed in the MTLE patients’ temporal lobe cortex, suggesting that it might be involved in the formation of abnormal neuronal networks.