摘要
目的观察海人酸(KA)诱导的癫疒间持续状态(SE)大鼠海马CA3区神经元线粒体与细胞核超微结构的损伤及caspase-3表达的变化。方法用KA诱导大鼠SE 2 h。分别于SE终止后第3 h、12 h、24 h取海马CA3区制作切片,光镜下观察神经元的变化,电镜下观察线粒体和细胞核的超微结构;免疫组化方法检测相同部位caspase-3的表达变化。结果光镜下SE后24 h神经元出现排列散乱、胞体皱缩、胞浆红染以及胞核固缩。电镜下SE后3 h,可见线粒体嵴肿胀及膜的崩解;SE后24 h细胞核染色质明显边聚。Caspase-3平均阳性细胞数及灰度值于SE后12 h较正常对照组显著增加(均P<0.05);24 h出现极显著增加(均P<0.01)。结论SE后早期海马神经元线粒体损伤可能是神经元损伤的关键环节。
Objective To observe the mitochondrion and nucleus ultrastructural damage and caspase-3 expression in hippocampal CA3 neurons during kainic acid （KA） induced status epilepticus （SE） in rats. Methods SE was induced for 2 h with KA in adult male Wistar rats. 3, 12 and 24 h later the rats were killed and the hippocampal CA3 subareas were taken out to make brain sections. The neuronal damage on the whole with light microscope and the uhrastructure of mitochondrion and nucleus with electron microscope. Caspase-3 expression of the same area was examined with immunohistochemical staining. Results 24 h after SE, by the light microscope examination, the KA group showed that the neurons put scattered disorder and nucleus shrink firmly. 3 h after SE, electron microscope examination showed swelling cristae and ruptured membrane of mitochondria. The change of nucleus were significant margination of chromatin 24 h after SE. Compared to normal control group, the caspase-3 expression increased 12 h after SE, the average number of positive cell and the gray scale were obviously higher （all P 〈0. 05 ） ; 24 h after SE, the results were more noticeable（ all P 〈 0.01 ）. Conclusion The ultrastructural damage of mitochondrion occurs in the early period after SE in rats, which may be critical in neuronal damage.
出处
《临床神经病学杂志》
CAS
北大核心
2006年第6期429-431,共3页
Journal of Clinical Neurology
基金
山东省自然科学基金资助(Y2001C10)
