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目的观察海人酸诱导的癫痫间持续状态(status ep ilepticus,SE)大鼠海马CA3区神经元线粒体损伤及caspase-3的表达。方法用海人酸诱导大鼠SE 2 h;于SE终止后第3、6、24 h取海马,光镜观察神经元的变化,并用电镜进一步观察线粒体的超微结构;免疫组化方法检测caspase-3的表达。结果SE终止后3h电镜下可见到线粒体嵴的肿胀和膜的崩解;SE后24 h神经元呈坏死样改变;caspase-3的表达在SE后6 h开始增加(与对照组比较,P<0.05),于第24 h明显增高(P<0.01)。结论在实验性SE模型中早期即出现线粒体超微结构的损伤,其后出现caspase-3的表达增高及神经元形态的改变,提示线粒体的损伤是SE后神经元损伤的关键环节。
Objective To observe the mitochondrial damage and the expression of caspase-3 in hippocampal CA3 region of hippocampus induced by kainate-induced status epilepticus (SE) in rats. Methods Kainic acid was used to induce SE 2 h in rats. The hippocampus was harvested at 3, 6 and 24 h after SE termination. The changes of neurons were observed under light microscope. The ultrastructure of mitochondria was observed by electron microscopy. The expressions of caspase -3 expression. Results The mitochondrial cristae swelling and membrane disintegration were observed under the electron microscope 3 h after SE termination. The neurons showed necrotic changes at 24 h after SE. The expression of caspase-3 began to increase at 6 h after SE (P < 0.05), and significantly increased at 24 h (P <0.01). Conclusion In the experimental SE model, mitochondrial ultrastructural damage occurs early, followed by increased expression of caspase-3 and changes in neuronal morphology, suggesting that mitochondrial damage is the key link of neuronal damage after SE.