A Preliminary Study About The Hippocampal Neural Apoptosis In The Mice Of Delayed Amnesia Induced By Carbon Monoxide Poisoning

Background:Carbon monoxide poisoning is a common cause of poisoning disease in modern life, which is harmful to health and life. Most of patients can resume through right therapy. But unfortunately a part of patients pass through the acute period, and go by a " false recover period ", which often last from several days to weeks, may reappear a series of encephalopathy symptoms, this phenomenia is called "delayed encephalopathy after carbon monoxide poisoning",which usually includes amnesia,consciousness, pyramid,extrapyramid disorder. So far the mechanism of delayed encephalopathy after carbon monoxide poisoning has been not clear, which is urgent to be solved.Object: Select the mice of delayed amnesia induced by carbon monoxide poisoning, detect the hippocampal neural apoptosis and the expression of Bax,Bcl-2 gene, and observe the pathological change. The ultimate purpose is to probe the mechanism of delayed encephalopathy after carbon monoxide poisoning, and supply a new train of thinking to cure delayed encephalopathy after carbon monoxide poisoning.Material and method: The mice carbon monoxide poisoning model was established with injecting 99.9%CO into abdominal cavity, and observe 80 health mices, memory capacity through the passive avoidance task up to one month,at last we select 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, at the same time, prepare pathological slice. At last we compare the difference among the control group, acute carbon monoxide poisoning group, delayed amnesia after carbon monoxide poisoning group.Results:1.The number of delayed amnesia mice is 8;the rate of delayed amnesia is 10%。2.Delayed amnesia after carbon monoxide poisoning group mices appear fade.tardy,memory impairment .3.The concentration of COHb of delayed amnesia after carbon monoxide poisoning group mices is normal.4.Compared with the control group, the number of the hippocampal neural apoptosis in delayed amnesia group elevated generously(P<0.01), and the expression of Bax/Bcl-2 gene is also elevated generously(P<0.05).5.Brain pathological change: the number of neuron cell in Hippocampal in delayed amnesia group decreased generously.Conclusion:1.We succeed in probing the variation pattern of memory impairment after carbon monoxide poisoning in mice, and establish the basis of the model of delayed encephalopathy after carbon monoxide poisoning.2.The research showed that neuron cell apoptosis in hippocampal is associated with delayed memory impairment after carbon monoxide poisoning in mice.3.The research evidenced that neuron cell apoptosis play an important role in delayed encephalopathy after carbon monoxide poisoning.