摘要
目的 :探讨托吡酯对戊四氮癫模型大鼠大脑的神经保护作用及可能的机制。方法 :成年雄性Wistar大鼠 5 4只 ,随机分为 :正常对照组 ( 6只 ) ;戊四氮组 ( 2 4只 ) ;托吡酯预处理组 ( 2 4只 )。癫发作后分别于 6、12、48h后处死取脑 ,进行HE染色和bcl 2、bax免疫组化染色。结果 :性发作后海马HE染色显示 ;戊四氮组CA1、CA3和DC区神经元变性及坏死较托吡酯预处理组显著。免疫组化染色显示 :托吡酯预处理组bcl 2 12和 48h在CA1、CA3和DC的表达强于戊四氮组 ,而bax在上述时段的表达则较戊四氮组弱。结论 :托吡酯具有一定的神经保护作用 ,推测可能与其增强大鼠海马神经元bcl 2基因表达 ,降低bax基因表达有关。
Aim:To explore the neuroprotective effect of topiramate and the possible mechanisms.Methods:54 adult male Wistar rats were randomly divided into blank control group(n=6),Pentetrazole-treated group(n=24),topiramate plus Pentetrazole treated group(n=24).Rats in the latter two groups were put to death and the brains were taken in patch 6 hours,12 hours,and 48 hours after seizures occurred.The hippocampi were studied histologically with HE staining and immunohistochemically for the expression of bcl-2 and bax.Results:Neuronal degeneration and necrosis in CA1,CA3,and DC areas of the hippocampi were more remarkable histologically in the pentetrazole-treated group than that in the topiramate plus Pentetrazole treated group.The expression of bcl-2 was more apparent in topiramate plus Pentetrazole treated group than that in Pentetrazole-treated group,whereas the expression of bax was less than that in Pentetrazole-treated group.Conclusion:Preconditioning with topiramate has no influence on epileptic attacks induced by Pentetrazole,but has neuroprotective effect,which might be related with the enhanced expression of bcl-2 genes and decreased expression of bax genes brought by the application of topiramate.
出处
《中国临床神经科学》
2004年第3期268-271,共4页
Chinese Journal of Clinical Neurosciences
