皮质注射氯化亚铁建立外伤性癫痫动物模型致痫机制的探讨

Mechanisms of Fe Cl_2-induced Post Traumatic Epilepsy Model on Rats

目的:皮质注射氯化亚铁(Fe Cl2)致外伤性癫痫(PTE)动物模型,探讨Fe Cl2致痫的可能机制。方法:成年SD大鼠24只随机分为正常组和模型组,各12只。通过注射Fe Cl2制作PTE模型,观察各组癫痫发作的行为、脑电图及病理表现,RT-PCR法检测海马及额叶c-fos,c-jun及c-myc m RNA转录水平。结果:模型组在行为学及脑电图表现均接近临床癫痫发作;模型组中c-fos、c-jun m RNA转录水平与正常组差异无统计学意义(P>0.05);模型组中c-myc m RNA转录水平显著高于正常组(P<0.01)。结论:Fe Cl2皮质注射制作PTE的机制可能与c-myc m RNA转录水平的升高有关。

Objective： To establish Fe Cl2-induced post traumatic epilepsy（PTE） model, and to explore the possible mechanisms. Methods： Twenty-four healthy adult SD rats were randomly divided into control group（n=12）and model group（n=12）. The PTE animal model was established by injecting Fe Cl2 into the cerebral cortex.Changes in behaviors, electroencephalograms（EEG） and histology of the hippocampus and frontal lobes were studied. The expression levels of c-fos, c-jun and c-myc m RNA were tested. Result： The behaviors and EEG of the rats in the model group were similar to the clinical feature of human epileptic seizures. There was no statistical difference in the expression levels of c-fos and c-jun m RNA between the normal control group and model group（P〉0.05）. As compared with the control group, the expression level of c-myc m RNA in the model group was increased significantly（P〈0.01）. Conclusion： The Fe Cl2-induced PTE model may be meditaed by the increase of the expression level of c-myc m RNA.