摘要
目的观察托吡酯(top iram ate,TPM)对红藻氨酸(kain ic ac id,KA)致癫痫持续状态(status ep ilepticus,SE)大鼠海马神经元凋亡的影响。方法取大鼠120只,随机分为TPM组、KA组及生理盐水(NS)对照组,每组再分为四个小组,分别用于SE后3、12、24和48 h四个时点。每小组10只大鼠。TPM组用TPM预处理。采用KA诱导大鼠SE。进行行为学评估、HE染色及TUNEL染色,并用免疫组化方法检测海马caspase-3的表达变化。结果TPM组大鼠的癫痫发作迟于KA组。HE及TUNEL染色显示,TPM组大鼠海马的病理损伤轻于KA组。免疫组化结果显示,TPM组caspase-3的表达明显低于KA组。结论TPM对KA诱导的SE发作具有抑制作用,并能显著降低海马caspase-3的表达,从而减轻癫痫所致的海马神经元损伤。
Objective To observe the effect of topiramate （ TPM ） on neuronic apoptosis following kainic acid （ KA ） induced status epilepticus （ SE ） in rats. Methods 120 adult male Wistar rats were randomly divided into three group- Group TPM, Group KA and the group of blank control. Every group was subdivided into four subgroups to leave to execute at 3 hours, 12 hours,24 hours and 48 hours after SE. There were 10 rats in every subgroup. Group TPM were pretreated with TPM. The behaviour was observed, HE staining and TUNEL stainings were made in rat after KA induced SE. The immunohistochemical staining was used to examine caspase-3 expression. Results Compared with group KA, the epileptic seizures were delayed in the group of TPM. HE and TUNEL staining revealed that the hippocampal pathological damage in group TPM was slighter than that in group KA. The immunohistochemical staining showed that the expression of caspase-3 was obviously down-regulated in Group TPM. Conclusion These results indicated that TPM may alleviate the seizure and reduce the expression of caspase-3 significantly. TPM could also lessen the hippocampal neuronic damage in SE rats.
出处
《滨州医学院学报》
2006年第4期244-246,共3页
Journal of Binzhou Medical University
