β-catenin在内侧颞叶癫痫发病机制中的作用

Role of β-catenin in the Pathogenesis of Mesial Temporal Lobe Epilepsy

目的探讨β-catenin与内侧颞叶癫痫发病机制之间的关系。方法以海人酸诱导建立内侧颞叶癫痫小鼠模型,采用Western blot检测正常鼠和模型鼠海马中β-catenin表达是否存在差异,免疫组织化学和免疫荧光技术检测非海马硬化内侧颞叶癫痫与海马硬化颞叶癫痫患者海马中β-catenin表达量是否存在差异。结果模型鼠海马硬化与内侧颞叶癫痫海马硬化相似,模型建立成功。Western blot检测结果显示,正常鼠与模型鼠海马的β-catenin表达无差异。免疫组织化学和免疫荧光检测结果发现,海马硬化患者的星型胶质细胞明显增多,β-catenin的表达量在非海马硬化颞叶癫痫和海马硬化颞叶癫痫患者间不存在差异。结论β-catenin可能未参与内侧颞叶癫痫海马硬化的形成过程。

Objective To explore the role of β-catenin in the pathogenesis of mesial temporal lobe epilepsy.Methods Kainic acid-induced rat models of medial temporal lobe epilepsy was established.The expression of β-catenin in the normal mice and the model mice were detected using Western blot analysis.The expression of β-catenin at human hippocampus was detected using immunohistochemical analysis and immunofluorescence and compared between patients with non-hippocampal sclerosis temporal lobe epilepsy and those with hippocampal sclerosis epilepsy.Results The pathologies of model mice were similar with those in mice with hippcampal sclerosis temporal lobe epilepsy,demonstrating that the mice model was successfully established.Western blot analysis showed no significant difference of β-catenin expression between normal mice and modelmice.As shown by immunohistochemical analysis and immunofluorescence,β-catenin expression in human hippocampus was also not significantly different between patients with temporal lobe epilepsy without hippocampal sclerosis and those with hippcampal sclerosis.Conclusion β-catenin may not be involved in the development of hippocampal sclerosis of mesial temporal lobe epilepsy.