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目的:研究匹罗卡品癫痫模型中海马区TREK-2双孔钾离子通道的表达变化,初步探讨TREK-2在癫痫发病过程中的机制及意义。方法:选用成年雄性SD大鼠腹腔注射氯化锂-匹罗卡品(lithium-pilocarpine)构建癫痫模型,分别在癫痫持续状态(status epilepticus,SE)后不同时间点(6 h、1 d、3 d、1 w、2 w、4 w、8 w)提取海马组织,利用western-blot检测海马区TREK-2随时间表达变化。并用TREK-2 si RNA下调海马区TREK-2表达,进一步观察对大鼠癫痫状态的影响。结果:与对照组相比,TREK-2在诱导癫痫持续状态发作后的3d开始降低(P<0.05),1 w,2 w,4 w明显降低(P<0.01),8 w时仍维持在很低水平(P<0.001)。在TREK-2表达下调后,大鼠癫痫潜伏时间(latent period)明显缩短,癫痫持续状态1 h 5级以上发作频率(seizure frequency)明显增加。结论:TREK-2在氯化锂-匹罗卡品致痫大鼠海马组织中表达的降低,且其下调加重癫痫状态的事实提示TREK-2参与了癫痫的发生发展过程。
Objective: To study the changes of TREK-2 double-hole potassium channel in hippocampus in pilocarpine epilepsy model and to explore the mechanism and significance of TREK-2 in the pathogenesis of epilepsy. Methods: Adult male Sprague-Dawley rats were injected intraperitoneally with lithium-pilocarpine to establish a model of epilepsy. The rats were sacrificed at different time points (6 h, 1 d, 3 h) after status epilepticus (SE) The changes of the expression of TREK-2 in the hippocampus with time were detected by western-blot. TREK-2 si RNA was used to down-regulate the expression of TREK-2 in hippocampus and further observe the effect on the status of epilepsy in rats. Results: Compared with the control group, TREK-2 decreased on the 3rd day after induction of epileptic seizure (P <0.05), significantly decreased at 1 w, 2 w and 4 w (P <0.01) Low level (P <0.001). After the down-regulation of TREK-2 expression, the latent period of epilepsy in rats was significantly shortened, and the seizure frequency was significantly increased at 1 h level 5 after epileptic seizure. CONCLUSIONS: The decreased expression of TREK-2 in the hippocampus of epileptic rats induced by lithium chloride-pilocarpine, and the fact that TREK-2 is down-regulated in the hippocampus suggests that TREK-2 is involved in the development of epilepsy.