急性一氧化碳中毒大鼠脑海马细胞凋亡及BAD蛋白的表达变化  

Brain hippocampus cellular apoptosis and change of the expression of BAD protein in rats after acute carbon monoxide poisoning

作　　者：穆永茂 王艳丽 李建民 王敏 张前进 

机构地区：[1]河北省迁安市人民医院重症医学科,河北唐山064400 [2]河北省迁安市人民医院神经外科,河北唐山064400

出　　处：《中医学报》2014年第B12期421-422,共2页Acta Chinese Medicine

摘　　要：目的研究急性一氧化碳中毒大鼠模型中海马细胞凋亡及BAD 蛋白在海马区的表达变化情况,为进一步预防和治疗一氧化碳中毒迟发性脑病提供理论依据.方法：选择取腹腔注射纯CO 制备急性一氧化碳中毒的大鼠模型.造模后分别于1、3、7、14、21d 处死,每个时间点8 只,对照组暴露于空气.断头取脑组织,采取TUNEL、免疫组化染色结合阳性细胞记数的方法观察大鼠海马区脑细胞凋亡情况及BAD 蛋白的表达的变化.并对所得数据进行统计学分析.结果：急性一氧化碳中毒7 d 大鼠脑海马凋亡细胞明显增加,第21 天达最高.Bad 蛋白表达显示海马区在第1 天表达明显,以后逐渐降低至染毒后21d,但仍高于对照组,与对照组相比差异有统计学意义（p〈0.01）,对照组BAD 蛋白表达无明显变化.结论：Bad 蛋白作为一种促凋亡因子表达活跃,可能是急性一氧化碳中毒迟发性脑病发生的病理机制之一.Objective To observe changes of apoptotic cells and the ex-pression of BAD protein in mice brain hippocampus after acute carbon monoxide poisoning.Methods：Rat model of acute carbon monoxide poisoning was induced by ip injected with CO repeatedly, then the brains of the CO exposed rats were taken after injection of CO 1、3、7、14 and21d with 8 rats at each time respectively. General TUNELand immunohistochemistry coup-led with computer-assisted image analysis were used to observe the neur-ological damageand changes of BAD protein expression.Results： The changes in BAD protein in hippocampus was rised rapidly after injection of CO, and reached max at 1d.being kept at higher levelfor long time till 21d. it was higher in the CO-exposed group than in the normal group （p〈0.01）. Conclusion： BAD protein expressed actively in acute carbon monoxidepoisoning,which maybe one of the mechanisms of delayed encephalopat-hy of carbon monoxide poisoning.

关 键 词：-氧化碳中毒 -氧化碳中毒迟发性脑病 BAD蛋白 凋亡 免疫组化 

分 类 号：R749.63[医药卫生—神经病学与精神病学]