摘要
目的观察海人酸(KA)诱导的癫痫持续状态(SE)大鼠海马CA3区神经元线粒体超微结构的损伤及caspase3的表达变化。方法用KA诱导大鼠SE2h。于SE终止后第3、12、24小时取海马,电镜观察线粒体的超微结构,免疫组化方法检测caspase3的表达。腹腔内注射生理盐水的大鼠设为对照组。结果SE终止后3h,电镜下可见线粒体肿胀及膜完整性的破裂。caspase3的表达于SE后12h较对照组增加,平均阳性细胞数及灰度值分别为10.49±0.68及45.57±2.27(P<0.05);于SE后24h,分别为37.36±0.57及115.24±1.22(P<0.01)。结论在实验性SE模型中,海马神经元线粒体超微结构的损伤早于caspase3的表达,提示线粒体的损伤可能是SE后神经元损伤的关键环节。
Objective To study the changes of mitochondrial uhrastructures and caspase-3 expression in hippoeampal CA3 neurons of rats with kainic acid （KA） induced status epilepticus （ SE）. Methods SE was induced with KA in adult male Wistar rats and was terminated with diazepam ：2 hrs later. The rats were sacrificed 3.14 and 24 hrs after SE and the brain sections were prepared. The mitochondrial uhrastructures were observed under an electron microscope. The immunohistochemical staining was used to examine caspase-3 expression. The rats that were injected with normal saline instead were used as the control group. Results E- lectron microscopy examination showed mitochondrion swelling and the membran ruptured in SE rats 3 hrs after SE. The caspase-3 expression increased in SE rats 12 hrs after SE compared with that in the control group. The average number of positive cells and the gray scale were 10.49 ± 0.68 and 45.57 ± 2.27 respectively, which were significantly higher than those of the control group （ 5.33 ± 0.43 and 19.79±0.33 ） （ P 〈 0.05 ）. Twenty-four hrs after SE, the caspase-3 expressinon increased more signifieantly, and the positive cells and the gray scale were 37.36±0.57 and 115.24±1.22 , respectively （P 〈 0.01 ）. Conclusions Mitochondrion was damaged and the caspase-3 expression increased in experimental SE. Mitochondrial damage appeared earlier than the increase of caspase-3 expression ,which suggested that mitochondrial damage might be critical in the process of neuronal injury after SE.
出处
《国际神经病学神经外科学杂志》
2005年第5期391-393,共3页
Journal of International Neurology and Neurosurgery
