托吡酯对海人酸致癫痫状态大鼠海马caspase-3表达的影响

观察海人酸（KA）诱导的癫痫持续状态（SE）大鼠海马区caspase 3表达的变化及托吡酯（TPM）对其的影响。方法：用TPM预处理；用KA诱导成年雄性Wistar大鼠SE模型。分别于SE终止后第3、12、24、48?h取脑，行HE染色做海马普通病理检查，并用免疫组化方法检测caspase 3的表达变化。结果：嗜酸性神经元在SE后24～48?h最多；caspase 3的表达亦于SE后同一时点明显增加；TPM在SE后24和48?h?点明显降低caspase 3的表达。结论：在实验性SE模型中，TPM可降低海马caspase 3的表达，从而减轻SE后脑损伤。

Effect of topiramate on caspase-3 expression in rat hippocampus following kanic acid induced status epilepticus

To observe the effect of topiramate (TPM) on the caspase 3 expression in rat hippocampus following kanic acid(KA)induced status epilepticus (SE). Methods: SE was induced in adult male Wistar rats following gastric injection TPM (18?mg/kg·d-1) and abdominal injection of KA(10?mg/kg), and 3, 12, 24 and 48 hours later, HE staining and immunohistochemical staining were used to examine the caspase 3 expression. Results: HE staining showed that acidophily neurons were the most in the period of 24～48?hours after SE, and caspase 3 expression increased significantly in the same period but declined at 24 and 48?hour time points by TPM. Conclusion: In experimental SE model, the caspase 3 expression increases 24 hours after SE but decreases by TPM, and therefore the brain damage is reduced.