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目的:探讨神经元凋亡与颞叶癫癎患者海马硬化的关系。方法:取15例颞叶癫癎患者手术切除标本(癫癎组)和5例无癫癎发作的患者正常脑组织标本(对照组),用原位末端标记(TUNEL)方法检测神经元凋亡,免疫组化染色检测细胞凋亡相关基因表达产物Bcl-2、Bax、Caspase-3蛋白的表达。结果:癫组和对照组的TUNEL阳性细胞平均百分率分别为(52.2±3.2)%、(4.0±1.8)%,差异有统计学意义(P<0.05)。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,癫癎组患者脑内Bcl-2蛋白表达明显增强(P<0.05);Bax蛋白在癫癎组与对照组中均微弱表达,差异无统计学意义;Caspase-3在对照组中有轻微表达,在癫癎组表达明显增强,差异有统计学意义(P<0.05)。结论:神经元凋亡部分参与癫癎患者海马硬化的形成,Bcl-2、Bax和Caspase-3蛋白在这一过程中可能发挥作用。
Objective: To investigate the relationship between neuronal apoptosis and hippocampal sclerosis in patients with temporal lobe epilepsy. Methods: Fifteen patients with temporal lobe epilepsy (epilepsy group) and 5 normal epilepsy patients (control group) were killed. Neuronal apoptosis was detected by TUNEL The expression of Bcl-2, Bax and Caspase-3 protein were detected by immunohistochemistry. Results: The average percentages of TUNEL positive cells in epileptic group and control group were (52.2 ± 3.2)% and (4.0 ± 1.8)%, respectively, with statistical significance (P <0.05). The results of immunohistochemistry showed that there was no expression of Bcl-2 protein in the control group, and the expression of Bcl-2 protein in the epileptic group was significantly increased (P <0.05). The levels of Bax protein in the epileptic group and the control group There was no significant difference between the two groups. Caspase-3 was slightly expressed in the control group and significantly increased in the epileptic group (P <0.05). CONCLUSION: Neuronal apoptosis is partly involved in the formation of hippocampal sclerosis in epileptic patients. Bcl-2, Bax and Caspase-3 proteins may play a role in this process.