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目的探讨高压氧治疗外伤性癫痫的机制。方法采用大脑皮层注射氯化亚铁建立外伤性癫痫大鼠模型,将癫痫大鼠分为无接受高压氧治疗的模型组及接受高压氧治疗的治疗组,将正常大鼠设立为正常组,对3组进行行为学观察及脑电图记录。取脑组织观察神经细胞形态改变,检测各组标本c-fos m RNA、c-jun m RNA、c-myc m RNA的表达水平。结果治疗组脑细胞形态学改变相对于模型组更少有神经元变性及凋亡。治疗组的c-jun m RNA、c-myc m RNA的表达水平较模型组明显下降(P<0.01)。结论高压氧治疗外伤性癫痫通过阻断c-jun、c-myc基因介导的细胞凋亡通路而起到治疗效果。
Objective To investigate the mechanism of hyperbaric oxygen therapy for traumatic epilepsy. Methods A rat model of traumatic epilepsy was established by injecting cerebral cortex with ferrous chloride. The epilepsy rats were divided into model group without hyperbaric oxygen therapy and treatment group with hyperbaric oxygen therapy. Normal rats were set as normal group. 3 groups for behavioral observation and EEG recording. The morphological changes of nerve cells were observed and the expressions of c-fos m RNA, c-jun m RNA and c-myc m RNA in each group were detected. Results The morphological changes of brain cells in the treatment group showed fewer neuron degeneration and apoptosis than the model group. The expression of c-jun m RNA and c-myc m RNA in the treatment group was significantly lower than that in the model group (P <0.01). Conclusion Hyperbaric oxygen treatment of traumatic epilepsy plays a therapeutic effect by blocking the apoptosis pathway mediated by c-jun and c-myc genes.