缝隙连接蛋白Cx43在SD大鼠电点燃癫痫模型中的表达

Expression of gap junction connexin43 in the SD rats electrical kindling of epilepsy model

目的探讨缝隙连接蛋白(Cx)在癫痫形成中的作用。方法将32只雄性SD大鼠随机分为4组,分别造模。观察SD大鼠行为,记录脑电图。通过免疫蛋白印迹的方法检测Cx43在大鼠海马区的表达变化。通过药物对癫痫电点燃模型成模过程的干预来观察癫痫形成与缝隙连接蛋白间的关系。结果模型组大鼠出现癫痫发作。蛋白印迹显示Cx43的表达异常增高。药物干预的2组SD大鼠模型痫性发作滞后,发作频率降低,程度减轻,痫性脑电波波幅降低,蛋白印迹显示Cx43的表达增高受到抑制。结论缝隙连接蛋白是癫痫形成的物质基础。抑制Cx43的过度表达,减少异常缝隙连接的形成,癫痫形成也受到抑制,从而预防癫痫产生。

Objective To investigate the role of connexin（Cx） in pathogenesis of epilepsy.Methods Thirty-two male SD rats were randomly divided into 4 groups and 4 models were set up.The behaviors of all SD rats were observed meanwhile the EEGs were recorded.Before the end Cx43 in hippocampus was detected with Western blot.The relationship between gap junction connexin and the formation of epilepsy was observed through the intervention of medicine to the kindling-model.Results Rats displayed typical epileptic behaviors,and epileptic discharges were observed in the epilepsy model group.The expression of connexin 43 in the hippocampal tissue was significantly enhanced in the epilepsy model group,but reduced by carbenoxolone and phenytoin sodium.Carbenoxolone and phenytoin sodium reduced frequency and amplitude of epileptic waves.The increasing expression of Cx43 was inhibited.Conclusion Gap junction Cx43 is the material base for the formation of epilepsy.The inhibition of excessive expression of Cx43 can reduce the formation of abnormal gap junction.Consequently the formation of epilepsy is inhibited.