Neuroprotective effect of oxaloacetate in rats with lithium-pilocarpine-induced epilepsy

吴兰香; 王果; 付利娟; 温纯洁; 杨竹; 王应雄; 于超

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Neuroprotective effect of oxaloacetate in rats with lithium-pilocarpine-induced epilepsy

更新时间：2026-01-09

- Neuroprotective effect of oxaloacetate in rats with lithium-pilocarpine-induced epilepsy
- Journal of Army Medical University Vol. 34, Issue 14, Pages: 1375-1379(2012)
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  CLC： R741.02;R742.1;R977.7
- Published：2012
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吴兰香,王果,付利娟,温纯洁,杨竹,王应雄,于超.草酰乙酸对锂-匹罗卡品癫痫大鼠的神经保护作用[J].陆军军医大学学报(原第三军医大学学报),2012,34(14):1375-1379.

　Wu Lanxiang,Wang Guo,Fu Lijuan,Wen Chunjie,Yang Zhu,Wang Yingxiong,Yu Chao.Neuroprotective effect of oxaloacetate in rats with lithium-pilocarpine-induced epilepsy[J].J Amry Med Univ (J Third Mil Med Univ),2012,34(14):1375-1379.
吴兰香,王果,付利娟,温纯洁,杨竹,王应雄,于超.草酰乙酸对锂-匹罗卡品癫痫大鼠的神经保护作用[J].陆军军医大学学报(原第三军医大学学报),2012,34(14):1375-1379. DOI：

　Wu Lanxiang,Wang Guo,Fu Lijuan,Wen Chunjie,Yang Zhu,Wang Yingxiong,Yu Chao.Neuroprotective effect of oxaloacetate in rats with lithium-pilocarpine-induced epilepsy[J].J Amry Med Univ (J Third Mil Med Univ),2012,34(14):1375-1379. DOI：

摘要

目的观察静脉注射草酰乙酸（oxaloacetate，OxAc）对氯化锂-匹罗卡品癫痫（lithium-pilocarpine seizures

LPS）模型大鼠的神经保护作用。方法 30只6～8周龄、体质量180～220 g的Sprague-Dawley雄性大鼠按随机数字表法分为5组：生理盐水对照组（用0.9%生理盐水代替匹罗卡品）、LPS模型对照组、LPS+OxAc组（癫痫持续状态终止时注射OxAc 3.5 mg/100 g）、LPS+OxAc+谷草转氨酶（glutamate-oxaloacetate transminase

GOT）组(癫痫持续状态终止时注射OxAc 3.5 mg/100 g+GOT 3.5 μg/100 g)及LPS+OxAc+马来酸盐（Maleate）组（癫痫持续状态终止时注射OxAc 3.5 mg/100 g+ Maleate 6.3 mg/100 g）（n=6）。用氯化锂和匹罗卡品制备癫痫动物模型，诱发癫痫持续状态（status epilepticus，SE）60 min后注射安定终止发作。分别检测SE终止后不同时间点各实验组大鼠脑脊液与血液中的谷氨酸浓度、脑电图表现及神经元脱失情况。结果 LPS模型对照组大鼠SE终止后脑脊液与血液中的谷氨酸浓度显著升高，8 h左右达到最高峰，与生理盐水对照组相比，分别升高了约88%和54%，随后开始缓慢下降。在SE终止后静脉注射OxAc可以在8 h内明显降低癫痫大鼠脑脊液中的谷氨酸浓度（P0.05），8 h后其作用基本消失；OxAc对癫痫大鼠血液中谷氨酸浓度的降低作用可以持续至注射后12 h（P0.05）。OxAc对癫痫大鼠脑电图表现及海马、齿状回门区神经元脱失现象也有明显改善作用。在应用OxAc的同时，静脉注射GOT可以增强OxAc对LPS大鼠的神经保护作用，而同时应用GOT特异性抑制剂Maleate可以减弱OxAc的上述作用效果。结论静脉注射OxAc可通过促使血液中谷氨酸浓度下降而对氯化锂-匹罗卡品癫痫模型大鼠的神经起到保护作用。

Abstract

Objective To observe the neuroprotective effect of intravenous oxaloacetate (OxAc) in a rat model of lithium-pilocarpine-induced epilepsy (LPE). Methods Thirty 6-8 weeks old male Sprague-Dawley rats

weighing 180-220 g

were randomly divided into control group

LPE model group

LPE+OxAc group

LPE+OxAc+glutamate-oxaloacetate transminase (GOT) group

and LPE+OxAc+maleate group

6 in each group. Rats in control group were given saline instead of pilocapine

rats in LPE model group and LPE+OxAc group were injected with OxAc at the dose of 3.5 mg/100 g when the seizure of epilepsy was arrested

rats in LPE+OxAc+GOT group were injected with OxAc at the dose of 3.5 mg/100 g and GOT at the dose of 3.5 μg/100 g when the seizure of epilepsy was arrested

and rats in LPE+OxAc+maleate group were injected with OxAc at the dose of 3.5 mg/100 g and maleate at the dose of 6.3 mg/100 g when the seizure of epilepsy was arrested. Sixty minutes after a rat epilepsy model was induced with lithium-pilocarpine

seizure of epilepsy was arrested by injecting diazepam. Glutamate level in cerebrospinal fluid and blood was measured

findings on electroencephalogram（EEG）and neuronal loss in different experimental groups were recorded at different time points. Results The level of glutamate in cerebrospinal fluid and blood was about 88% and 54% higher in LPE model group than in control group after the seizure of epilepsy was arrested (P0.05）and reached its peak at 8 h

then began to decrease slowly

indicating that intravenous OxAc could significantly reduce the glutamate level in cerebrospinal fluid and blood within 8 and 12 h after the seizure of epilepsy was arrested (P0.05）. OxAc could also significantly improve the EEG and neuronal loss in hippcampus and dentate hilus. Intravenous GOT could improve the neuroprotective effect of OxAc

while maleate (a specific inhibitor of GOT) could attenuate the neuroprotective effect of OxAc in rats with epilepsy. Conclusion Intravenous OxAc exerts its neuroprotective effect in rat LPE model by down-regulating the glutamate level in blood.

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