颞叶癫痫患者致痫灶中凋亡调控基因Bcl-2和Bax的表达

Expressions of apoptosis regulatory genes Bcl-2 and Bax in human temporal lobe epilepsy

目的探讨神经元凋亡与颞叶癫痫患者海马硬化的关系。方法取16例颞叶癫痫患者手术切除标本,用光镜、电镜及原位末端标(TUNEL)方法检测神经细胞凋亡;应用免疫组化方法检测细胞凋亡相关基因表达产物Bax和Bcl-2蛋白的表达。结果对照组患者光镜、电镜检查及TUNEL染色均未发现凋亡的神经细胞;癫痫组患者光镜检查及TUNEL染色未发现凋亡的神经细胞,但在电镜检查的3例标本中,1例有少量早期凋亡征象的神经元。免疫组化染色结果表明,对照组患者脑组织内Bcl-2蛋白无表达,癫痫组患者脑内Bcl-2蛋白表达明显增强(P<0.001);Bax蛋白在癫痫组与对照组中均微弱表达,两者差异无统计学意(P>0.05)。结论神经元凋亡部分参与了癫痫患者海马硬化的形成,Bcl-2和Bax蛋白在这一过程中可能发挥了作用。

Objective To explore the relationship between neuron apoptosis and hippocampus sclerosis of human temporal lobe epilepsy. Methods The specimens were obtained from 16 patients with temporal lobe epilepsy. Neuron apoptosis was investigated by light microscopy, electron microscopy and TdT-mediated dUTP-biotin nick end labeling （TUNEL） method,and the expression of Bcl-2, Bax was determined by immunohistochcmistry. Results The evidence of neuron apoptosis was not found by light microscopy, electron microscopy and TUNEL method in control group. But some early signs of neuron apoptosis in 3 patients（ 3/8 ）were found by electron microscopy in epilepsy group. Unlike that in normal adult brain,Bcl-2 immunoreactivity was observed in some neurons in epilepsy group（ P 〈 0. 001 ） compared with normal group. Bax immunoreactivity was not increased in epilepsy group （ P 〉 0. 05 ）. Conclusion Neuron apoptosis is involved in hippocampus sclerosis of human epilepsy. Bcl-2 and Bax protein may play a role in this process.