Hippocampal neuronal apoptosis in rats caused by delayed encephalopathy after acute carbon monoxide poisoning and expression of Erk1/2 and Bad protein
AIM:To investigate hippocampal neuronal apeptosis in model rats and expression of extra cellular signal regulated protein kinase 1/2(Erk1/2)and Bcl-2/Bcl-xl-associated death promoter(Bad)protein,and to study the possible pathogenesis of delayed encephalopathy after acute carbon monoxide poisoning (DEACMP).METHODS:Male 48 SD rats(240-280 g),were randomly divided into the control group and the carbon monoxide (CO)-poisoned group(1,3,7,14,21 d after poisoning).The latter were injected in abdominal cavity with CO in several times to establish DEACMP model.The symptoms of rats after poisoning were observed and the concentration of carboxyhemoglobin(COHB)in rats'caudal vein were monitored dynamically.The hippocampal tissues of each group were taken to prepare paraffin pathological section and hematoxylin-eosin(HE)staining,TdT-mediated dUTP nick end labeling(TUNEL),immunohistochemical method were used to observe morphological changes in the hippocampal area,the amount of apoptotic cells and expression of Erk1/2 and Bad protein.RESULTS:CO-poisoned rats were in the coma state for a long time.and COHB were kept at higher level(>50%)for longer time(>16 h);apparent hippocampal neuronal degeneration and necrosis occurred on the 7th-14th day after poisoning;the amount of apeptotic cells also reached the highest level on the 7th-14th day(P<0.05);the expression level of Erk1/2 protein decreased gradually during 1 st-21st day (P<0.05);and the expression of Bad protein increased on the 1 st day and peaked on the 3rd day,then decreased,and still kept higher level than that of the control group even at the 21 st day (P<0.05).CONCLUSION:The expression level of Erk1/2 decreased and that of Bad increased with a following decline after CO poisoning,which indicates that Erk1/2 and Bad protein attribute to hippocampal neural apoptosis and are involved in the pathogenesis of DEACMP.
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