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采用HE、TUNEL和免疫组织化学法 ,观察急性一氧化碳中毒脑损伤与凋亡的关系。发现急性一氧化碳中毒可引起小鼠大脑皮层、海马、纹状体等部位脑细胞凋亡 ,凋亡细胞在中毒 3天后明显增加 ,5～ 7天达到高峰 ,14天后恢复正常 ;同时可以诱导促凋亡基因Fas、FasL蛋白表达 ,表达高峰在中毒后 3～5天 ,早于凋亡发生时间。由此可看出急性一氧化碳中毒可以诱导脑细胞凋亡及Fas、FasL表达 ,中毒所致迟发性脑病可能与脑细胞凋亡有关
HE, TUNEL and immunohistochemistry were used to observe the relationship between brain injury and apoptosis in acute carbon monoxide poisoning. Found that acute carbon monoxide poisoning can cause cerebral cortex, hippocampus, striatum and other parts of brain cells apoptosis, apoptotic cells significantly increased after 3 days of poisoning, 5-7 days to reach the peak, returned to normal after 14 days; at the same time can induce pro-apoptotic Fas gene expression of Fas, FasL protein expression, expression peak 3 to 5 days after poisoning, as early as the time of apoptosis. It can be seen that acute carbon monoxide poisoning can induce apoptosis of the brain cells and Fas, FasL expression, poisoning-induced delayed encephalopathy may be related to brain cell apoptosis