【摘要】 目的研究癫痫患者脑组织中突触后密度-93(PSD-93)mRNA的表达,探讨其在癫痫形成中的作用。方法将56例癫痫患者分成耐药和非耐药两组,首先用基因芯片对其术后标本进行扫描,并与对照组比较,随后对目标基因PSD-93用逆转录聚合酶链反应(RT-PCR)技术进行验证。结果基因芯片检测发现与依赖N-甲基-D-天门冬氨酸受体(NMDARs)-一氧化氮(NO)信号有关的基因PSD-93在癫痫患者中表达上调,RT-PCR实验结果与基因芯片一致。RT-PCR电泳图的灰度值均数在对照组为23.577、非难治性癫痫组为56.931、难治性癫痫组为51.607,非难治性、难治性癫痫组与正常对照组灰度的比值中位数分别为2.415、2.189(P<0.05),而非难治性与难治性癫痫组灰度值比值为1.103(P>0.05)。结论脑细胞膜相关鸟苷酸激酶家族(MAGUK)蛋白信号转导复合体的分子接头蛋白基因PSD-93mRNA表达增加,其可能通过信号传导异常及神经元坏死参与了癫痫的形成。更多还原

【Abstract】 Objective To investigate the expression of postsynaptic density-93(PSD-93) mRNA in the brain tissues from the patients with epilepsy so as to explore the possible mechanisms of the pathogenesis of the epilepsy. Methods A total of 56 patients with epilepsy were divided into intractable epilepsy (IE) and non- intractable epilepsy (NIE) groups. Differences of their gene expression were evaluated by cDNA microarray compared with non-epileptogenic control. Then the expression of PSD-93 mRNA was detected by reverse transcription polymerase chain reaction (RT-PCR). Results cDNA microarray analysis showed that the mRNA expression of PSD-93, which correlated with the function of N-methyl-D-aspartate receptors (NMDARs)-nitric oxide (NO) signal transduction pathway, was significantly higher in epilepsy patients than those in the control group. The results of RT-PCR were consistent with the cDNA microarray data. The mean gray levels of electrophoresis in patients of non-epileptogenic control, NIE and IE groups were 23.577, 56.931 and 51.607 respectively after RT-PCR. The median of ratio of gray level was 2.415, 2.189 (P<0.05) in patients of NIE and IE compared with control group respectively. However, the median of ratio of NIE and IE was 1.103 (P>0.05).Conclusion The upregulated mRNA expression of PSD-93, which belongs to the adaptor protein of MAGUK (membrane associated guanylate kinase) protein complex in brain tissue, may be involved in the pathogenesis of epilepsy by impairment of signal transduction and death of neurons.更多还原