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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 ,尤其是后期的发生和发展中起着重要作用
Objective To explore the molecular and pathological mechanism of refractory epilepsy by understanding the differential expression of homologous mitochondrial genes between resistant and non-phenytoin sodium (PHT) epileptic mice. Methods The PHT-resistant and non-drug resistant epilepsy rat model was established. The mR NA was extracted from brain tissue by routine extraction and cDNA was reverse transcribed. After cDNA was reverse transcribed and labeled with cDNA microarray containing 4096 human known genes, 37 genes and mitochondria related genes in the difference between the two expression. RESULTS: Twelve of the 37 genes in brain mitochondria of PHT-resistant mice were abnormally expressed. Conclusions Abnormal expression of mitochondrial genes in brain cells may be the molecular pathological basis of refractory epilepsy. Energy metabolism disorders and neuronal apoptosis play an important role in the formation of refractory epilepsy, especially in the later stage