一氧化碳中毒迟发记忆障碍小鼠海马神经细胞凋亡的初步研究

Preliminary study about hippocampal neural apoptosis in mice of delayed amnesia induced by carbon monoxide poisoning

关键词:  一氧化碳中毒  迟发记忆障碍  海马神经细胞凋亡  凋亡调控基因

Key words:  Carbon monoxide poisoning  hippocampal neural apoptosis  delayed amnesia  apoptosis gene

摘要:

［目的］通过对一氧化碳中毒迟发记忆障碍小鼠海马神经细胞凋亡的研究， 探索一氧化碳中毒迟发脑病的发病机制。［方法］ 筛选出急性中毒记忆受损恢复后又再一次出现记忆保持能力下降的迟发记忆障碍小鼠 , 测其海马神经细胞凋亡及其调控基因 Bax 、 Bcl-2 表达。［结果］急性一氧化碳中毒小鼠中有 10% 出现迟发记忆障碍，迟发记忆障碍小鼠血浆碳氧血红蛋白正常；其海马神经细胞凋亡显著增加(P<0.01)；凋亡调控基因 Bax/Bcl-2 值增加 (P<0.05) 。［结论］一氧化碳中毒小鼠迟发记忆障碍与其海马神经细胞凋亡具有相关性 , 神经细胞凋亡在迟发性脑病的发病机制中起着重要的作用。

Abstract:

［Objective］ In the preliminary study about hippocampal neural apoptosis in mice of delayed amnesia induced by Carbon monoxide poisoning ,we investigated the mechanism of delayed encephalopathy after carbon monoxide poisoning. ［Method］ Observe a part of mice, which appear a curve of recover to descend on memory. Blood was obtained by orbital artery and vein to measure the concentration of COHb, and utilize fluroscene technology to identify the hippocampal neural apoptosis and the expression of Bax 、Bcl-2 gene. ［Results］ The percent of delayed amnesia after actue carbon monoxide poisoning was 10%,the concentration of COHb of delayed amnesia after carbonmonoxide poisoning group mices was normal.Compared with the control group, the number of the hippocampal neural apoptosis in delayed amnesia group elevated generously, and the expression of Bax/Bcl-2 gene is also elevated generously. ［Conclusion］ The results above showed that neuron cell apoptosis in hippocampal is associated with delayed memory impairment after carbon monoxide poisoning in mice.Neuron cell apoptosis plays a important role in the mechanism of delayed encephalopathy after carbon monoxide poisoning.