活化蛋白-1在急性一氧化碳中毒迟发性脑病大鼠海马的表达变化

Study of changing levels of AP-1 in hippocampus of delayed encephalopathy after acute carbon monoxide poisoning rats

目的:观察急性一氧化碳中毒后不同时间点大鼠海马AP-1的表达变化。方法:腹腔注射一氧化碳的方法制备一氧化碳中毒迟发性脑病模型,HE染色观察大鼠海马区病理变化,免疫组化及Western blot法检测AP-1的表达水平,TUNEL染色计数海马CA1区凋亡神经元。结果:HE染色,空气组(AC组)、空白组(BC组)各时间点海马区细胞形态正常;一氧化碳组(CO组)海马区细胞肿胀、细胞数目减少,排列紊乱,细胞间隙扩大,细胞核碎裂、深染、固缩。免疫组化:CO组各时间点AP-1表达量均高于AC组及BC组,3 d达峰值,组内第3天与其余各时间点比较差异有统计学意义(P<0.05)。Western blot:AP-1表达在时间分布趋势上与免疫组化结果一致。TUNEL染色:CO组各时间点凋亡指数均较AC组、BC组多,于毒染后7 d达高峰差异有统计学意义(P<0.05)。结论:大鼠海马区AP-1表达增高,可能进一步导致细胞凋亡和炎症免疫反应,成为DEACMP发病的重要机制之一。

Objective：To investigate the levels of AP-1 in hippocampus of rats at different time points after carbon monoxide poisoning.Methods： Carbon monoxide poisoning delayed encephalopathy model by using intraperitoneal injection of carbon monoxide.Uesd HE observed the pathological changes in hippocampus of rats.The levels of AP-1 was observed by immunohistochemistry and Western blot analysis.TUNEL was used to detect apoptotic neurons in hippocampal CA1 area.Results： HE dyeing conditions,the hippocampus cell of air group （AC） and blank group （BC） were normal at each time point.Pathological changes occurred in the hippocampus cell of Carbon monoxide group （CO）,reduction in the number of cells,disorder of cells,intercellular space expansion,nuclear fragmentation,anachromasis and pyknotic.Immunohistochemical results,the AP-1 expression level at each time point in group CO were higher than group AC and BC.On 3th day it reached a peak.The comparison at all time points among the groups in the first three days were significantly different in statistics（P〈0.05）.Western blot results,the expression of AP-1 was consistented with the immunohistochemical results on the time distribution trend.TUNEL results,AI in group CO was higher than those in group AC and BC at all time points,there were significant differences（P〈0.05） and 7th reached the peak of apopotsis.Conclusion： Inside the hippo-campus of rats,there are increasing in AP-1.Maybe it is one of the important pathogenesis of DEACMP .