中文摘要：

目的：观察白介素1B（IL-1β）与核因子-KB（NF-KB）在大鼠内侧颞叶癫痫（mesial temporal lobe epilepsy，MTLE）模型中的表达变化；体外培养的星形胶质细胞经IL-1β和吡咯烷二硫氨基甲酸（PDTC）预处理后，观察其增殖和NF-κB表达变化。方法：利用匹罗卡品诱导sD大鼠发作癫痫制成MTLE模型，根据自发发作出现和稳定时间分为急性期对照组（AC，制模后2h）、急性期癫痫组（AS）、潜伏期对照组（LC，制模后3周）、潜伏期癫痫组（LS）、慢性期对照组（CC，制模后8周）和慢性期癫痫组（cs）。体外培养的星形胶质细胞分为对照组、IL组和PDTC＋IL组，利用凝胶迁移电泳（EMSA）、免疫印迹（WB）、酶联免疫吸附（ELISA）和免疫组织化学（IHC）的方法观察IL-1β和NF-κB的表达变化；MTr检测星形胶质细胞的增殖活化程度。结果：匹罗卡品诱导的MTLE模型大鼠海马内IL-1β和NF-κB在急性期、潜伏期和慢性期表达均增加，但以急性期和慢性期明显；IL-1β可以促进体外培养的星形胶质细胞增殖、上调星形胶质细胞内NF-κB的表达，而PDTC可以明显抑制IL-1β的上述作用。结论：IL-1β通过NF-κB促进大鼠星形胶质细胞的活化增殖，这一改变可能与MTLE发病密切相关，探讨其机制可能为MTLE的治疗提供新的靶点。

英文摘要：

Objective： To observe the expression changes of IL-1β and NF-κB in the different stages of mesial temporal lobe epilepsy（MTLE） model on rats, and the proliferation and expression change of NF-κB in astrocyte after pretreating with IL-1β and PDTC in vitro. Methods： The SD rat MTLE models were established by Pilocarpine. According to the spontaneous seizure and stable time, the rats were divided into acute stage control group （AC）, acute stage seizure group （AS）, latent stage control group （LC）, latent stage seizure group （LS）, chronic stage control group （CC） and chronic stage seizure group （CS）. Astrocyte was cuhured in vitro and divided into control group （C）, IL-1β group （IL）, PDTC and IL-1β group （P ＋ IL）. The expression changes of IL-1β and NF-κB were detected by electrophoretic mobility shift assay（ EMSA）, Western blot, ELISA and immunohistochemistry. The activation and proliferation of astrocyte were detec- ted by MTr. Results： The expression of IL-1β and NF-κB increased in all three stages of MTLE rats＇ models, especially in acute and chronic stages. The proliferation of astrocyte and the expression of NF-κB in astrocyte were promoted by IL-1β after stimulating in vitro. And these were inhibited by PDTC obviously. Conclusion： Via NF-κB, the activation andproliferation of astrocyte were increased by IL-1β. This change may be related with the pathogenesis of MTLE, and new target for the treatment of MTLE may be provided by the discussion of its mechanism.