隐源性难治性颞叶癫癇患者脑内丝裂原活化蛋白激酶激酶激酶5基因表达的研究

Study of MAPKKK5 gene expression of brain tuissur in patients with cryptogenic refractory temporal lobe epilepsy

目的检测丝裂原活化蛋白激酶激酶激酶5(MAPKKK5) mRNA及其编码蛋白产物在隐源性难治性颞叶癫癇(TLE)患者脑内的表达,从分子水平探讨难治性TLE可能的发病机制。方法取10例隐源性难治性TLE患者手术切除的颞叶组织,10例脑外伤患者(病例对照组)相应部位颞叶组织,利用RT-PCR与Westernblot方法检测两组患者MAPKKK5 mRNA(MAPKKK5 mRNA/β-actin)与MAPKKK5蛋白(MAPKKK5/β-actin)的表达。结果难治性TLE患者颞叶组织MAPKKK5 mRNA(1.001±0.321)和MAPKKK5蛋白(0.359±0.299)的表达水平均上调,与病例对照组的(0.648±0.157)和(0.137±0.084)比较差异有统计学意义(均P<0.05)。结论MAPKKK5基因表达上调可能参与难治性TLE的发病机制。

Objective To verify the variation of mitogen-activated protein kinase kinase kinase 5 （ MAPKKK5 ） gene expression in patients with cryptogenic refractory temporal lobe epilepsy （TLE） and to evaluate the possible molecular pathogenesis of intractable TLE. Methods Reverse transcription polymerase chain reaction （RT-PCR） and Western-blot analysis were used to measure the expression alterations of MAPKKK5 mRNA as well as its protein product MAPKKK5 in temporal cortex samples from patients who had undergone temporal lobectomy for intractable epilepsy （n = 10）. Tissues from 10 subjects who did not have epilepsy served as controls. Results The expression of MAPKKK5 mRNA （ 1. 001 ± 0. 321 ） and its protein MAPKKK5 （ 0. 359 ± 0. 299） were significantly increased in epileptic brain compared with the controls （0. 648 ± 0. 157, 0. 137 ± 0. 084, respectively） （all P〈 0. 05 ）. Conclusion Up-regulation of MAPKKK5 expression might be a potential etiological agent for refractory TLE.