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目的研究连接蛋白32在颞叶癫患者病变海马组织中的表达,从而为癫的发病机制进一步提供理论依据。方法14例颞叶癫(伴海马硬化)患者手术切除的病变海马组织为癫组,8例因其他疾病死亡进行尸检者的正常海马组织为对照组,死者生前无癫发作,利用免疫组织化学与蛋白印迹检测(Western-blot)方法检测两组连接蛋白32的表达水平,并进行比较。结果应用免疫组织化学方法检测发现对照组连接蛋白32有比较低的水平表达,但在癫患者的海马组织中表达增强,差异有显著性(P<0.01);应用Western-blot方法检测发现对照组连接蛋白32有低水平表达,在癫患者的海马组织中表达明显增强,差异有非常显著性(P<0.001)。结论颞叶癫患者海马组织中连接蛋白32表达增高,缝隙连接在癫的发生、发展过程中可能起到了重要作用。
Objective To study the expression of connexin 32 in the hippocampus of patients with temporal lobe epilepsy and to provide a theoretical basis for the pathogenesis of epilepsy. Methods Fourteen patients with temporal lobe epilepsy (with hippocampal sclerosis) underwent surgical resection of the hippocampus in the epilepsy group. Eight of the normal hippocampus patients who died of other diseases were selected as the control group, and the deceased was born without epileptic seizures. Histochemistry and Western blotting were used to detect the expression of connexin 32 in two groups and compared. Results The expression of connexin 32 in control group was lower than that in control group (P <0.01) by immunohistochemistry. However, the expression of connexin 32 in control group was significantly higher than that in control group (P <0.01) The expression of Connexin32 was low in hippocampus of patients with epilepsy, and the difference was significant (P <0.001). Conclusion The expression of connexin 32 in hippocampus of patients with temporal lobe epilepsy is increased, and the gap junction may play an important role in the occurrence and development of epilepsy.