1,6-二磷酸果糖对急性一氧化碳中毒致小鼠脑损伤的治疗作用  

Therapeutic Effect of 1,6-Fructose-diphosphate on Cerebral Injury Induced by Acute Carbon Monoxide Poisoning in Mice

作　　者：赵晓辉[1] 杨俊卿[1] 周岐新[1] 石全红[2] 

机构地区：[1]重庆医科大学药理教研室,重庆400016 [2]重庆医科大学临床学院脑外科,重庆400012

出　　处：《工业卫生与职业病》2003年第6期342-346,共5页Industrial Health and Occupational Diseases

基　　金：重庆市科委中青年科技专家基金 ( 99-3 3 -2 )

摘　　要：目的　研究 1 ,6 -二磷酸果糖 (FDP)对急性一氧化碳 (CO)中毒致小鼠脑损伤的治疗作用。方法　小鼠单次腹腔注射CO 1 70ml/kg,以CO中毒小鼠死亡率 ,被动回避性记忆能力、脑细胞膜和线粒体膜Ca2 + Mg2 + ATPase活力、脑组织单氨氧化酶B (MAO B)活力、海马病理形态学的改变为指标 ,研究FDP对急性CO中毒致小鼠脑损伤的治疗作用。结果　FDP以剂量依赖性的方式降低CO中毒小鼠的死亡率 ,明显改善CO中毒小鼠记忆能力的下降 ,显著阻遏CO中毒小鼠脑细胞膜和线粒体膜Ca2 + Mg2 + ATPase活力的病理性降低以及脑组织MAO B活力的病理性升高 ,并能一定程度避免海马神经元损伤。此治疗作用以CO中毒 1 5min内给予FDP最为明显。Objective To study the therapeutic effects of 1,6 fructose diphosphate (FDP) on delayed cerebral injury in mice followed after acute CO exposure.Methods Mice were exposed to CO( 170 ml/kg ip)once.After the exposure,mortality of mice,changes of memory function in passive avoidance test,pathomorphological observation of brain tissue slices,and changes of monoamine oxide(MAO) B and Ca 2+ Mg 2+ ATPase activities in cerebral tissue were observed.FDP(LD,MD,HD)was administrated 15 min after CO exposure,and FDP (MD) was administrated 0,15,45,and 120 min after CO exposure.Results FDP could obviously decrease the mortality of mice,distinctively conserve the impairment of memory function,prevent the delayed cell death in hippocampal neurons and hinder the rising of MAO B activity and the decreasing of Ca 2+ Mg 2+ ATPase induced by acute CO poisoning in dose\|and time dependent manner.Conclusions These results suggest that FDP might have therapeutic effects on delayed cerebral injury in mice induced by acute CO exposure.

关 键 词：急性一氧化碳中毒 脑损伤 治疗作用 1 6-二磷酸果糖 小鼠 

分 类 号：R135.14[医药卫生—劳动卫生]