| 高琴琴 王晖 刘明富 江涛 刘昕乐 肖昭扬.匹罗卡品癫痫模型中海马区TREK-2 钾离子通道表达变化及意义[J].,2015,15(3):449-452 |
| 匹罗卡品癫痫模型中海马区TREK-2 钾离子通道表达变化及意义 |
| Expression Changes and Meaning of TREK-2 PotassiumIon Channel inHippocampus in Pilocarpin-induced EpilepsyModel |
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| DOI： |
| 中文关键词: TREK-2 氯化锂-匹罗卡品 癫痫 |
| 英文关键词: TREK-2 Lithium-pilocarpine Epilepsy |
| 基金项目:国家自然科学基金项目(81071052；81471373) |
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| 中文摘要: |
| 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 siRNA 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。 |
| 英文摘要: |
| Objective:To investigate the expression change of K2P channel TREK-2 in hippocampus with pilocarpin-induced
epilepsy, and to explore the mechanism and siginificance of epilepsy in which TREK-2 was involved.Methods:The epilepsy model was
conducted by celiac injection of lithium-pilocarpine with adult male Sprague-Dawley rats, the hippocampus tissue was collected
respectively at 6 h, 1 d, 3 d, 1 w, 2 w, 4 w and 8 w after the status epilepticus (SE), and the expression changes of TREK-2 in
hippocampus was detected at different time points with Western-Blot. The expression of TREK-2 was down-regulated in hippocampus
with TREK-2 siRNA, and the effect on status epilepticus (SE) was further observed.Results:Compared to control group, the expression
of TREK-2 began to decrease at 3 d (P < 0.05), decreased significantly at 1 w, 2 w, 4 w, (P< 0.01), and remained a very low level at 8 w
(P < 0.001). After the expression of TREK-2 declined, the latent period of epilepsy decreased significantly, and the seizure frequency of
SE significantly increased within 1 h above magnitude 5.Conclusion:The decreased expression of TREK-2 potassium ion channel in
hippocampus in pilocarpin-induced epilepsy model and the down-regulated TREK-2 which aggravated the status epilepticus indicated
that TREK-2 participated in the ocurrence and development of epilepsy. |
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