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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。
Objective To study the expression of post-synaptic density-93 (PSD-93) mRNA in epileptic brain tissue and to explore its role in epilepsy. Methods Fifty-six patients with epilepsy were divided into drug-resistant and non-drug-resistant groups. The samples were scanned by gene chip and compared with the control group. Then the target gene PSD-93 was reverse transcriptase polymerase chain reaction -PCR) technology to verify. Results Gene microarray detection showed that PSD-93, a gene related to N-methyl-D-aspartate receptor (NO) signal, was up-regulated in epileptic patients. The results of RT-PCR Gene chips are identical. The average gray value of RT-PCR in the control group was 23.577, non-refractory epilepsy group was 56.931, refractory epilepsy group was 51.607, non-refractory, refractory epilepsy group and the normal control group gray value ratio The median was 2.415 and 2.189 respectively (P <0.05), while the gray value of non-refractory and refractory epilepsy was 1.103 (P> 0.05). Conclusion The increase of PSD-93 mRNA expression in brain cell membrane-associated guanylate kinase family (MAGUK) signaling transduction complex may play an important role in the development of epilepsy through abnormal signal transduction and neuronal necrosis.