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。
[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.
出处
《中国医学工程》
2007年第4期338-340,344,共4页
China Medical Engineering
基金
教育部高校青年教师奖(教人司2001-182)
国家自然科学基金(30500172)
