| Abstract:Objective:To observe the expression of hypoxia-induciblefactor-1alpha(HIF-1α) and Fas protein in hippocampus of rats after acutecarbon monoxide poisoning,and explore the possible role of them in thepathogenesis of delayed encephalopathy after acute carbon monoxidepoisoning(DEACMP).Methods:78male SD rats (250g~320g) were randomlydivided into three groups:blank control group(BC group)(n=18),sham-operatedgroup (n=30)and delayed encephalopathy after acute carbon monoxidepoisoning group(CO group)(n=30).The time points of1st,3rd,7th,14th,21thand28thday after acute carbon monoxide poisoning were set for measuring the changes.The rats in CO group were injected in abdominal cavity with pure CO severaltimes to establish DEACMP model,rats in sham group were injected equal air bysame way,BC group without any treatment.Morris water maze test was used tomeasure the learning ability and memory such as the average escaped latency,time during platform quadrant and number of passing through platform.Thepathological change at hippocampal gyrus of rats brain was observed byH-E.The apoptosis of pyramidal neurons at hippocampal gyrus area wasmeasured by TUNEL.The expression of hypoxia-inducible factor-1alpha(HIF-1α) and Fas in hippocampal area was measured byimmunohistochemistry.Results:1.Morris water maze test:The average escaped latency of rats in three groups were no statistically significant difference beforepoisoning,and it has no statistically significant difference among different timepoint in BC group and Sham group.The average escaped latency of rats in COgroup were increased after poisoning,and there were remarkable statisticallysignificance at14th,21thand28thday after poisoning compared with rats in othertwo groups(P<0.01).The time during platform quadrant of rats in three groupswere no statistically significant difference before poisoning,and it has nostatistically significant difference among different time point in BC group andSham group.It was shorten in CO group rats after poisoning,and there werestatistically significance at14thand28thday after poisoning compared with othertwo groups(P<0.05).The number of pass through platform was no statisticallysignificant difference in three group rats before poisoning,and it has nostatistically significant difference among different time point in BC group andSham group.It was decreased in CO group rats after poisoning,and there werestatistically significance at28thday after poisoning compared with other twogroups(P<0.05).2.Pathological changes:Neuronal cells edema, nuclear pyknosis,nuclear fragmentation, number of neurons reducing and other pathologicalchanges were shown in rats brain after acute carbon monoxide poisoning.Thepathological changes of the brain tissue in sham-operated group and BC groupwere not obvious.3.Examination result of apoptosis:The apoptosis of pyramidalneurons in hippocampal gyrus was found increased since3rd day after the COpoisoning, and it was reached the peak at7thday，and it still had a few apoptosis at28thday. The apoptotic index in CO group was increased significantlycompare with BC group and sham-operated group (P＜0.01).4.Result ofimmunohistochemistry:1) Expression of HIF-1α：The expression of HIF-1αinhippocampal gyrus was found increased since1stday after the COpoisoning,reached the peak at3rdday,and it still had a high expression at28thday.The expression in CO group was increased significantly compare with BCgroup and sham-operation group(P＜0.01).2)Expression of Fas protein:Theexpression of Fas protein in hippocampal gyrus was found increased since1stday after the CO poisoning,and reached the peak at3rdday,then begin todecrease at7thday,there were remarkable statistically significance comparedwith other two groups at1st,3rd,7thand14thday(P＜0.01).Conclusion:1.Intraperitoneal injection of pure CO to establish DEACMP modelis easy to operate,and it has the similar pathophysiological process with humandelayed encephalopathy after acute carbon monoxide poisoning, it is the idealmodel for DEACMP study.2.Morris water maze experiment is mainly used fortesting the learning and memory ability for space position of experimentalanimals,it can be used as a reliable basis of judging DEACMP occurred in ratsafter CO poisoning.3. Hypoxia-inducible factor-1alpha(HIF-1α)may playan important role in delayed encephalopathy after acute carbon monoxidepoisoning(DEACMP) by inducing the apoptosis of neurons in hippocampalgyrus area.4.Hypoxia-inducible factor-1alpha(HIF-1α) may induce theapoptosis of neurons in hippocampus by upgrade the expression of Fas protein. |
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