辛伐他汀抑制海人酸模型大鼠癫痫发作  

Administration of Simvastatin after epileptic seizures induced by Kainic Acid restrains chronic temporal lobe epilepsy of rats

作　　者：谢春成[1] 沈红[1] 浦松[1] 刘利[1] 林志国[1] 

机构地区：[1]哈尔滨医科大学附属一院神经外科,150001

出　　处：《中华神经外科杂志》2013年第1期26-29,共4页Chinese Journal of Neurosurgery

基　　金：国家自然科学基金（81071215）;黑龙江省卫生厅科研课题（2011-018）;黑龙江省中医药科研项目（ZHY12-Z135）;黑龙江省自然科学基金面上项目（1）201216）;黑龙江省博士后科研启动基金（LBH-Q11041）

摘　　要：目的研究辛伐他汀（Sire）抑制海人酸（KA）诱导的大鼠抽搐发作向颞叶癫痫（TLE）发展的长期影响。方法将大鼠分为健康对照组、盐水治疗癫痫组、Sim治疗癫痫组。KA诱导癫痫半小时后，Sire灌胃。（1）大鼠抽搐后3d评估了细胞因子（TNF-α、IL-1β、IL-6）的水平变化。（2）在4—6个月观察海马胶质细胞增生、神经元死亡、苔状纤维发芽（MFS）和大鼠癫痫发作情况。结果Sim降低了TNF-α、IL-1β水平，减轻了胶质细胞增生和神经元死亡，并抑制了海马MFS和癫痫发作。结论Sire具有抑制KA诱导的大鼠急性抽搐发作向TLE发展的效能。Objective To examined the effect of the chronic administration of Sire immediately after epileptic seizure in rat brains with temporal lobe epilepsy （TLE）. Methods （ 1 ） We evaluated cytokine expressions 3 days post KA - lesions in the hippocampus. （2） We quantified reactive astroeytosis and neuron loss in the hippocampus at 4 - 6 months after KA - lesions. We then assessed aberrant mossy fiber sproutings （MFS） in the epileptic brain. Seizure scores were recorded 4 to 6 months after KA - lesions. Results We found that Sim - treatment suppressed lesion - induced expressions of tumor necrosis factor - α（ TNF - α） and interleukin （IL） - 1β, suppressed reactive astrocytosis, and attenuated loss of neurons in the hippocampus. In contrast to the robust MFS observed in the saline - treated animals, Sim restrained the extent of MFS in epileptic rats. There was also a trend toward improvement in seizure scores. Conclusion Our study suggests that Sim administration might be a possible intervention and promising strategy for the prevention of SE intensifying to become chronic epilepsy.

关 键 词：辛伐他汀 细胞因子类 神经胶质增生 癫痫 颞叶 大鼠 

分 类 号：R742.1[医药卫生—神经病学与精神病学]