摘要
目的：观察拉莫三嗪（LTG）及丙戊酸钠（VPA）对锂-匹罗卡品癫痫持续状态（SE）大鼠海马锥体细胞、齿状回门区神经元的保护作用及对癫痫的治疗作用。方法：用大鼠制作锂-匹罗卡品SE动物模型，分三组：SE对照组，LTG治疗组和VPA治疗组。此三组在SE后2h给予安定阻断痫性发作，再分别给予适量生理盐水（NS）、LTG、VPA治疗15d，比较各组海马锥体细胞、门区神经元计数、继发癫痫的发生率及苔藓纤维出芽的评分。另设有正常对照组（NS组），不制模只给予NS“治疗”。结果：SE对照组、LTG组及VPA组齿状回门区均出现神经元丢失，VPA组及SE对照组均存在海马CA1神经元丢失，但LTG组海马CA1锥体神经元无丢失；三个模型组继发癫痫的发生率及苔藓纤维出芽的评分比较差异无统计学意义。结论：锂-匹罗卡品SE模型中，SE2h后给药，LTG能够对大鼠海马锥体细胞起到神经保护作用，VPA无明显保护作用，但两种抗癫痫药物均不能够阻断癫痫的发生及齿状回苔藓出芽。
Objective： To observe neuroprotection of lamotrigine （LTG） and valproate sodium （VPA） to hippocampal pyramidal cells and hilal neurons and their effects on the secondary seizures in lithiam pilocarpine induced status epilepticus（SE） model, and to investigate the neuroprotection of antiepileptic drugs. Methods： Lithium pilocarpine SE animal model was made with,rats and diazapam, LTG, VPA were individually administrated 2h after SE to interrupt seizures. Various groups were individually given NS,LTG,VPA trentment for 15 days so as to observe and analyse the number of hippocampal pyramidal cells and hilal neurons, the rate of the secondary epilepsy and scores of mossy fiber sprouting. Then the NS control group was treated with NS, without model making. Results： Hilai neuron loss was found in SE control group, LTG group and VPA group. There was no hippocampal pyramidal cell loss of CA1 subregion in LTG group, whereas obvious neurons loss was found in VPA and SE control group. No statistical differernce was found in the rate of the secondary epilepsy and scores of mossy fiber sprouting of the three groups. Conclusion： LTG can exert neuroprotection to hippocampal pyramdical cells 2 h after SE in lithium-pilocarpine SE model, whereas VPA cannot exert neuroprotection, but both antiepileptic drugs cannot prevent from epileptogenesis and mossy fiber sprouting.
出处
《癫痫与神经电生理学杂志》
2011年第2期65-69,共5页
Journal of Epileptology and Electroneurophysiology(China)
