摘要
目的观察内向整流钾离子通道亚单位基因KCNJ4mRNA及其编码的蛋白产物Kir2·3在难治性颞叶癫患者和急性脑外伤患者脑内的表达差异,从分子水平探讨难治性颞叶癫可能的发病机制。方法12例难治性颞叶癫患者手术切除的颞叶组织,10例急性脑外伤患者相应部位颞叶组织,利用逆转录-聚合酶链反应(RT-PCR)与蛋白印迹检测(Western-blot)方法检测两组间KCNJ4mRNA(KCNJ4mRNA/β-actin)与Kir2·3通道蛋白(Kir2·3/β-actin)的表达。结果难治性颞叶癫患者与脑外伤患者比较,颞叶组织KCNJ4mRNA(0·438±0·178)及Kir2·3通道蛋白(0·063)的表达水平均降低,差异有统计学意义(P<0·05)。结论KCNJ4mRNA表达水平的下调及其编码产物Kir2·3通道蛋白表达水平的下降,可能是难治性颞叶癫发生发展的重要的分子学基础之一。
Objective To evaluate the possible molecular pathogenesis of intractable temporal lobe epilepsy. The potassium ion channel gene KCNJ4 encodes one of the subfamilies of Kir channels, Kir2. 3 subunit, which may play an important role in modulating neuronal exeitation. Interference in the function or expression of this gene would cause disturbance of ionic concentrations, thus leading to seizure activity. Methods Reverse transcription polymerase chain reaction （RT-PCR） and Western-blot analysis were used to measure the expression alterations of KCNJ4 mRNA as well as its protein product Kir2. 3 channel in temporal cortex samples from patients who had undergone temporal lobectomy for intractable epilepsy （n = 12）. Tissue from 10 subjects who did not have epilepsy served as controls. Results The expression of KCNJ4 mRNA （ 0. 438 ± 0. 178 ） and its protein Kir2. 3 （ M50 = 0. 063 ） were significantly decreased in epileptic brain compared with the controls （ P 〈 0.05 ）. Conclusion The variation in KCNJ4 expression might be a potential etiological agent for TLE that may offer a novel target for antieonvulsant therapy.
出处
《中华神经科杂志》
CAS
CSCD
北大核心
2006年第4期242-245,共4页
Chinese Journal of Neurology
关键词
癫癎
颞叶
钾通道
内向整流
基因表达
Epilepsy, temporal lobe
Potassium channels, inwardly-rectifying
Gene expression
