中文摘要：

观察大鼠癫痫持续状态后线粒体融合分裂相关基因Mfn2和Drp1在海马中的动态变化,探讨线粒体融合分裂在癫痫发生中的作用. 随机将成年雄性Wistar大鼠48只分为对照组、癫痫持续状态（status epilepticus,SE）后2h、8h及24 h组,后3组建立氯化锂-匹鲁卡品诱导的大鼠癫痫持续状态模型.观察各组大鼠行为学变化;采用Nissl染色检测海马神经元损伤;采用实时定量PCR（real time quantitativePCR,QT-PCR）方法观察大鼠海马Mfn2及Drp1 mRNA表达变化. ①与对照组相比,SE组可见大鼠海马CA1和CA3区细胞正常结构破坏、神经元脱失等改变,以癫痫发作后24 h最显著.②与对照组相比,SE后Mfn2 mRNA表达均较对照组显著降低（F=5.362,P=0.006）,而Drp1 mRNA表达均较对照组显著升高（F =6.655,P=0.002）. 线粒体融合分裂失平衡可能是造成癫痫神经损伤的重要原因.

英文摘要：

Objective： To investigate the changes of expression of mitochondrial fusion and fission- associated genes Mfn2 and Drpl in the hippocampus of pilocarpine-treated rats, explore the role of mitochondrial fusion and fission in epilepsy. Methods： 48 adult male Wistar rats were randomly divided into control group and 2 h, 8 h and 24 h after status epilepticus （SE） groups. The SE model was induced by lithium-pilocarpine through intraperitoneal injection. Behavioral episodes in epileptic rat were observed and hippocampal neuron death was examinedby Nissl staining. The changes of Mfn2 and Drpl mRNA levels were detected by real time quantitative PCR （QT-PCR）. Results： （1）Nissl staining showed that normal cell structure was destroyed and nerve cells were lost in CA1 and CA3 regions of hippocampal in SE group, especially at 24 h after SE. （2）The level of Mfn2 mRNA was significantly decreased, while the level of Drpl mRNA was significantly increased after SE compared with control group. Conclusion ： The unbalance of mitochondrial fusion and fission may be critical in the process of neuronal injury after SE.