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目的观察凋亡基因caspase-10在外伤性癫痫病灶中的表达变化,探讨其作用机制。方法收集外伤性、非外性癫痫患者手术切除的脑皮质及交通事故死亡者脑皮质各15例,运用RT-PCR技术观察比较各实验组凋亡基因caspase-10表达水平,采用荧光免疫组织化学染色技术观察各实验组凋亡基因对应蛋白的表达情况。结果外伤性癫痫组caspase-10基因和蛋白表达水平比非外伤性癫痫组和交通事故死亡组高,差异有统计学意义(P<0.05);非外伤性癫痫组caspase-10基因和蛋白表达水平亦显著高于交通事故死亡组(P<0.05)。结论凋亡基因caspase-10能促进神经元凋亡,对外伤性癫痫的发病过程有促进作用。
Objective To observe the change of apoptosis gene caspase-10 in traumatic epilepsy and to explore its mechanism. Methods Totally 15 cases of cerebral cortex were collected from patients with traumatic and non-external epilepsy. The expression of caspase-10 in each experimental group was observed by RT-PCR. The expression of caspase-10 was detected by fluorescence immunohistochemistry Dyeing technique was used to observe the expression of the corresponding proteins of apoptotic genes in each experimental group. Results The levels of caspase-10 gene and protein in traumatic epilepsy group were significantly higher than those in non-traumatic epilepsy group and traffic accident death group (P <0.05). The levels of caspase-10 gene and protein in non-traumatic epilepsy group were significantly higher than those in non-traumatic epilepsy group Also significantly higher than the traffic accident death group (P <0.05). Conclusion Apoptosis gene caspase-10 can promote neuronal apoptosis and promote the pathogenesis of traumatic epilepsy.