中文摘要：

目的探讨白介素1-beta（IL-1β）在大鼠内侧颞叶癫痫（MTLE）模型病情进展中的作用,并探讨其与核因子-κB（NF-κB）的作用关系。方法利用匹罗卡品诱导SD鼠发作癫痫制成MTLE模型,并于制模成功后0.5h侧脑室注射IL-1β,于慢性期（8w）,利用行为学观察、脑电图检测观察模型鼠自发癫痫的情况,利用Nissl染色和Timm染色观察模型鼠海马神经元脱失和苔藓纤维增生情况;利用凝胶迁移电泳（EMSA）和免疫组化（IHC）观察海马内NF-κB和NF-κB p65的表达。结果 IL-1β可以提高匹罗卡品诱导的MTLE模型鼠慢性期自发癫痫的发生率,且加重海马内神经元脱失和苔藓样纤维增生,并且NF-κB表达增加,与对照组和单纯匹罗卡品诱导组比较均有统计学差异（P〈0.05）。结论 IL-1β通过NF-κB促进匹罗卡品诱导的MTLE模型鼠癫痫慢性自发发作,是导致MTLE进展的机制之一。

英文摘要：

Objective To understand the effect of IL-1B in the progress of MTLE in rat model and discuss the rela- tionship between IL-1β and NF-κB. Method The rats were divided into control group, pilocarpin group （Model I group）, pilocarpin and IL-1β group （Model 11 group）. The rats in Model Ⅰ group were intraperitoneally injected pilocarpin （50rag/ kg） to induce status epilepticus. The rats in model Ⅱ group were intracerebroventricularly injected IL-1β （10ng/kg） after SE induced by Pilocarpine. The rats were fed for 8 weeks. Detect the spontaneous recurrent seizures （SRS） were detected by behavior observation and electroencephalogram （EEG）. Nissl stain was used to observe the losses of neuron. Timm stain was used to observe the proliferation of Mossy fiber. Electrophoretic mobility shift assay （EMSA） and immunohistochemistry were used to detect the expressions of NF-κB and NF-κB p65 in each group. Results IL-1β improved exacerbated the loss of neuron and the proliferation of Mossy fiber, increased the morbidity of SRS and the expression of NF-κB in rat model of MTLE （ P 〈 0.05 ）. Conclusion IL-1β could promote the occurrence of SRS in rat model of MTLE by NF-κB pathway.