摘要
目的 通过了解耐 /非耐苯妥英钠 (PHT)癫痫鼠与人类同源线粒体基因的差异表达来探索难治性癫痫的分子病理机制。方法 建立PHT耐药和非耐药癫痫鼠模型 ,取脑组织常规抽提mR NA ,逆转录生成cDNA并标记后 ,与含有 4 0 96条人类已知基因的cDNA表达谱芯片杂交 ,检测线粒体内 37个基因及线粒体外相关基因在两者间的差异表达。结果 发现耐PHT鼠脑线粒体 37条基因中有12条基因表达异常。结论 脑细胞线粒体基因表达异常可能是难治性癫痫的分子病理基础 ,能量代谢障碍和神经元凋亡在难治性癫痫形成 。
Objective To explore the molecular mechanism of intractable epilepsy through the differential expression of mitochondrial genes in brains between the phenytoin resistant and non resistant epileptic rats.Methods After establishing phenytoin resistant and non resistant epileptic kindling models,Wistar rats were sacrificed.The mRNAs were extracted from their brains and were reversely transcribed to cDNAs as hybridization probes which were hybridized with BioDoor4096 cDNA microarray.Then the differentially expressed genes related to mitochondria between the two groups were analyzed by ImaGene3 0 software. Results The results showed that 12 genes were lower expressed among 37 mitochondrial genes and genes related to mitochondria in the resistant epilepsy rat group. Conclusions The mitochondrial genes expressed abnormally in brains may be the basic mechanism of molecular pathology in refractory epilepsy. The apoptosis and the decreased energy metabolism of neurons may play an important role in the formation and development of refractory epilepsy.
出处
《中华神经外科杂志》
CSCD
北大核心
2002年第4期234-237,共4页
Chinese Journal of Neurosurgery
