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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。
Objective: To investigate the neuroprotective effects of topiramate on brain of pentylenetetrazol epilepsy model rats and its possible mechanism. Methods: 54 adult male Wistar rats were randomly divided into four groups: normal control group (n = 6), pentylenetetrazol group (n = 24) and topiramate pretreatment group (n = 24). After epileptic seizures, the brains were sacrificed at 6, 12 and 48 hours after the onset of epilepsy. HE staining and bcl 2 and bax immunohistochemical staining were performed. Results: HE staining of hippocampus after 发 seizure showed that degeneration and necrosis of neurons in CA1, CA3 and DC of pentylenetetrazole group were more significant than those of topiramate pretreatment group. Immunohistochemical staining showed that the expression of bcl 2 and 48h in topiramate preconditioning group was stronger than that of pentylenetetrazolium group in CA1, CA3 and DC, while the expression of bax was weaker than that in pentylenetetrazole group. Conclusion: Topiramate has some neuroprotective effects, suggesting that it may be related to the enhancement of bcl 2 gene expression and the decrease of bax gene expression in rat hippocampal neurons.