摘要
目的探讨癫痫持续状态(statusepilepticus,SE)大鼠海马神经元损伤与氧化应激的关系。方法采用匹罗卡品(pilocarpine,PILO)诱导大鼠SE模型,用Nissl染色和TUNEL染色观察海马神经元损伤;用比色法检测海马丙二醛(malondialdehyde,MDA)、还原型谷光甘肽(glutathione,GSH)的水平以及谷光甘肽还原酶(glutathionereductase,GR)的活力。结果SE后6h,大鼠海马可见少量TUNEL标记细胞;SE后48h,TUNEL阳性细胞明显增多,至SE后72h达到高峰;SE后7d,TUNEL阳性细胞数量明显减少。大鼠海马MDA含量在SE后6h迅速升高,并达到高峰;SE后48￣72h,海马MDA含量虽比SE后6h有所降低,但仍明显高于对照组,差异有显著性(P<0.01);SE后7d,海马MDA含量基本恢复正常。GSH含量和GR活力在SE后6h迅速降低;SE后48h降至最低点;SE后72h￣7d,海马GSH含量虽较SE后48h有所升高,但仍显著低于对照组(P<0.01);海马GR活力于SE后72h开始升高,至SE后7d基本恢复正常。结论PILO诱导的海马神经元死亡包括坏死和凋亡两种形式,氧化应激机制参与了PILO诱导的海马神经元损伤。
[Objective] To study the correlation between hippocampal neuronal damage in epileptic rats and oxidative stress. [Methods] Use model of status epilepticus (SE) induced by pilocarpine. Neuronal damage in hippocampus was detected by Nissl staining and TdT-mediated dUTP Nick End Labeling (TUNEL) staining, and the level of malondialdehyde (MDA), glutathione (GSH) and glutathione reductase (GR) activity were observed by colormetric method. [Results] At 6 h post-SE, the number of TUNEL positive neurons begin to increase and peak at 72 h post-SE. The number of TUNEL positive neurons begin to decrease at 7 d post-SE. At 6h post-SE, the level of MDA increased rapidly and reached peak. At 48~72 h post-SE, the level of MDA begin to decrease, but was still significantly higher than the controls (P <0.01). At 7 d post-SE, the level of MDA dropped to normal level. At 6 h post-SE, the level of GSH and GR activity decreased rapidly and touched bottom at 48 h post-SE, at 72 h^7 d post-SE, the level of GSH begin to increase, but was still significantly lower than the controls (P <0.01). At 72 h post-SE, GR activity begin to increase and come back to normal at 7 d post-SE. [Conclusion] Neuronal death in hippocampus in epileptic rats induced by pilocarpin includes necrosis and apoptosis. Oxidative stress is involved in hippocampal neuronal damage in epileptic rats induced by pilocarpine.
出处
《中国现代医学杂志》
CAS
CSCD
北大核心
2006年第24期3690-3693,共4页
China Journal of Modern Medicine
关键词
癫痫持续状态
海马
氧化应激
匹罗卡品
凋亡
status epilepticus
hippocampus
oxidative stress
pilocarpine
apoptosis
