中文摘要：

目的动态观察颞叶癫痫大鼠神经元磷酸化Akt（phospho-Akt）蛋白的表达变化，探讨其在癫痫发生发展中的作用。方法清洁级SD雄性成年大鼠36只，随机分为正常对照组、诱发大鼠癫痫持续状态（statusepilepticus，SE）后3h、6h、12h、24h、3d组。用氯化锂LiCl和匹罗卡品（PILO）制备癫痫动物模型，应用免疫组织化学染色技术检测致痫后各时间点磷酸化Akt蛋白表达情况。结果免疫组织化学法显示正常组与假手术组大鼠海马CA1、CA3区可见少量磷酸化Akt阳性细胞，两组间差异无统计学意义（P〉0.05）；模型组可见CA1、CA3区Akt阳性细胞增加（P〈0.01），6h达到高峰，3d回到对照组水平。结论上调磷酸化Akt蛋白表达有利于减少海马神经元凋亡，可能是保护神经损伤的机制之一。

英文摘要：

[Objective] To observe the expression of phosphor-AKt-protein in hippocampus of rats with temporal lobe epilepsy consecutively and explore the possible effects on the development of epilepsy. [Methods] Thirty-six healthy adult male Sprague-Dawley （SD） rats were randomly divided into normal control group, 3 h group （3 hour after SE）, 6 h group （6 hour after SE）, 12 h group （12 hour after SE）, 24 h group （24 hour after SE）, and 3 d group （3 day after SE）. The lithium chloride （LiCL） and pilocarpine（PILO）-induced seizure model were established to evalulate the expression of phosphor-AKt-protein at each time-point after status epilepticus by immunohistochemistry. [Results] A small quantity of phosphor-AKt-positive ceils had been seen in CA1 and CA3 region of rats＇ hippocampus by immunohistochemistry in both normal control group and pseudo-operated group, whose differences had no statistical significance （P 〉0.05）; the number of phosphor-AKt-positive cells increased in CA1 and CA3 region of hippocampus in model group （P 〈0.01）, and it reached the peak after 6 hours and went back to the level of control group after 3 day. [Conclusion] Up-regulating the expression of phosphor-AKt-protein will decrease the apoptosis of hippocampal neuron, which may be one of mechanisms of protective nerve injury.