急性一氧化碳中毒大鼠迟发性脑损伤机制及地塞米松干预作用  

Mechanism of delayed encephalopathy after acute carbon monoxide intoxication in rats and intervention of dexamethasone

作　　者：项文平[1] 王宝军[1] 薛慧[1] 张军[1] 庞江霞[1] 

机构地区：[1]包头市中心医院神经内科,内蒙古包头014040

出　　处：《中华实用诊断与治疗杂志》2015年第3期231-234,共4页Journal of Chinese Practical Diagnosis and Therapy

基　　金：国家临床重点学科建设项目(2012)

摘　　要：目的探讨急性一氧化碳中毒大鼠迟发性脑损伤的病理机制及地塞米松对迟发性脑损伤的干预作用。方法健康雄性Wistar大鼠120只,随机分为中毒组、地塞米松组和对照组各40只。中毒组和地塞米松组采用腹腔内注射一氧化碳制备急性一氧化碳中毒模型,对照组注射等体积空气。地塞米松组在中毒后30 min内腹腔注射地塞米松30mg/(kg·d),共7d;中毒组和对照组腹腔注射等剂量生理盐水。采用Morris水迷宫评估3组大鼠智力状态,采用ELISA法检测中毒后90min和7、14、21d各组大鼠血清髓鞘碱性蛋白(myelin basic protein,MBP)、髓过氧化物酶(myeloperoxidase,MPO)表达水平,采用免疫组织化学法检测海马MBP、MPO阳性纤维表达情况。结果地塞米松组中毒后7、14d逃避潜伏期((23.0±3.0)、(22.5±1.5)s)较中毒组((104.5±9.0)、(63.5±2.5)s)明显缩短(P<0.05),与对照组((25.7±1.3)、(24.1±2.6)s)比较差异无统计学意义(P>0.05);中毒后90min、7、14、21d中毒组血清MBP水平((6.98±1.14)、(6.48±0.87)、(5.92±1.28)、(5.21±1.18)μg/L)较地塞米松组((4.98±1.72)、(4.56±0.70)、(4.60±0.74)、(4.12±0.68)μg/L)和对照组((3.81±1.11)、(3.68±0.81)、(3.83±0.71)、(3.82±1.01)μg/L)明显增高(P<0.05),地塞米松组与对照组比较差异无统计学意义(P>0.05);中毒后14d中毒组血清MPO水平((4.15±0.40)u/mL)较地塞米松组((1.64±0.30)u/mL)和对照组((0.99±0.80)u/mL)明显增高(P<0.05),地塞米松组与对照组比较差异无统计学意义(P>0.05);中毒组大鼠中毒后90min^21d可见脑海马MBP阳性纤维表达稀疏,地塞米松组MBP阳性纤维表达致密,接近于对照组;3组脑海马均无MPO表达。结论炎症反应在急性一氧化碳中毒大鼠迟发性脑损伤的发病机制中起重要作用,地塞米松通过有效抑制炎症反应所致髓鞘损害,减轻了急性一氧化碳中毒大鼠迟发性的脑损伤。Objective To investigate the potential mechanism of delayed encephalopathy after acute carbon monoxide poisoning in rats,and the effect of dexamethasone.Methods A total of 120 male Wistar rats were randomly divided into poisoning group,dexamethasone group and control group,with 40 rats in each group.Poisoning group and experimental group were intraperitoneally injected with carbon monoxide to establish animal models of acute carbon monoxide poisoning,while control group was injected with an equal volume of air.Dexamethasone group was intraperitoneally injected dexamethasone 30mg/（kg·d）within 30 min after poisoning,once a day,totally for 7days.Control group and poisoning group were intraperitoneally injected normal saline.Animal intelligence was assessed by Morris water maze experiment.The serum myelin basic protein（MBP）and myeloperoxidase（MPO）levels were detected by ELISA in 90 min,7days,14 days and 21 days after poisoning.The levels of MBP and MPO in hippocampus were measured by immunohistochemistry method.Results The average latencies on the 7th and 14 th days after poisoning were significantly shorter in dexamethasone group（（23.0±3.0）,（22.5±1.5）s）than those in poisoning group（（104.5±9.0）,（63.5±2.5）s）（P〈0.05）,and showed no significant difference in comparison with those in control group（（25.7±1.3）,（24.1±2.6）s）（P〉0.05）.The MBP levels 90 min,7days,14 days and 21 days after poisoning were（6.98±1.14）,（6.48±0.87）,（5.92±1.28）and（5.21±1.18）μg/L in poisoning group,significantly higher than those in dexamethasone group（（4.98±1.72）,（4.56±0.70）,（4.60±0.74）,（4.12±0.68）μg/L）and control group（（3.81±1.11）,（3.68±0.81）,（3.83±0.71）,（3.82±1.01）μg/L）（P〈0.05）,there were no significant differences between dexamethasone and control group（P〉0.05）.The MPO level 14 days after poisoning was higher in poisoning group（（4.15±0.40）u/mL）than that in dexamethasone group（（1.64±0.30�

关 键 词：急性一氧化碳中毒 髓鞘碱性蛋白 髓过氧化物酶 地塞米松 大鼠 

分 类 号：R595.1[医药卫生—内科学]