| Objective In this study,a mouse model of delayed encephalopathy(DEACMP)caused by carbon monoxide poisoning was established by static inhalation of CO,the damage of hippocampus tissue and the expression of Axl and Mer were observed,and its role in the pathogenesis of DEACMP was analyzed,thus providing certain theoretical basis for the pathogenesis and prevention of DEACMP.Methods Thirty-four F1 male adult mice born from 129 S2/Sv Pas and C57BL/6 mice were screened for cognitive function.Thirty-two mice were screened and randomly divided into experimental group(n=16)and control group(n=16).Mice in the experimental group were placed in a CO poisoning box and inhaled CO gas with a concentration of 3000 PPM for 40 min to establish a DEACMP mouse model,while mice in the control group were placed in an air-filled poisoning box for 40 min.experimental group mice were tested for COHb concentration at 15 min,30 min,l h,2 h and 4h after poisoning respectively.Morris water maze experiment was used to evaluate the cognitive function changes of mice 21 days after poisoning.The hippocampal tissue damage of mice was observed by HE staining,and the expression of Axl and Mer in hippocampal tissue was detected by Western Blot.Results Performance of mice in experimental group after acute CO poisoning:1.After acute CO poisoning,the symptoms were mild excitement and restlessness form 5 to 10 minutes,and increased respiratory frequency and deepened depth,dispirited spirit,limp limbs,cherry red mucous membrane of mouth,nose and claw,like to curl up in the corner,some of them suffered convulsions,coma,opisthotonus and death from 20 to 40 minutes.Autopsy of the dead mice revealed that the internal organs were hyperemic with scattered bleeding points and the brain tissues were seriously hyperemic and swollen.It is consistent with the manifestations of acute CO poisoning.As for the control group,the breathing was uniform,the mental state was well and the movement was free.There was no abnormal change.2.The changes of COHb after CO poisoning in the experimental group were dynamically monitored.The blood COHb content was increased and fluctuated between 33.5-53.0% 15 min after CO poisoning,and the COHb concentration in the experimental group gradually decreased with the extension of time after CO poisoning.3.Morris water maze test: Compared with the control group,the escape latency of mice in the experimental group was prolonged and the difference was statistically significant(P<0.05,t=22.659).4.HE dyed: In the experimental group,the number of hippocampal tissue cells and cell layers decreased,the cell structure was disordered,the cell shrinkage was obvious,and the structure was unclear.In the control group,hippocampal neurons were arranged orderly,with regular morphology and clear construction.5.Western Blot experiment: Compared with the control group,the content of Axl in the experimental group increased.It was statistically significant(P<0.05,t=2.971).Compared with the control group,the content of Mer increased significantly in the experimental group.It was statistically significant(P<0.05,t=2.234).Conclusion The content of Axl and Mer in TAM receptor increased obviously in hippocampus of DEACMP mice,which may play an important role in the pathogenesis of DEACMP. |
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