促红细胞生成素在大鼠急性一氧化碳中毒迟发型脑病中的表达及意义

摘要

目的 探讨促红细胞生成素(EPO)在大鼠急性一氧化碳中毒迟发型脑病(DEACMP)中的表达及意义.方法 将90只SD级雄性健康成年大鼠按简单随机化方法随机分为3组:空白对照组(BC组)、空气对照组(AC组)、DEACMP组.DEACMP组采用腹腔注射一氧化碳法建立DEACMP模型,AC组在腹腔内注射等量空气,BC组不作任何处理.将3个组按染毒后第1、3、7、14、21、28天分为6个亚组.运用Morris水迷宫实验检测大鼠认知行为学改变,TUNEL染色观察大鼠海马CA1区细胞凋亡情况,免疫组化染色观察大鼠海马CA1区EPO的表达.结果 DEACMP组大鼠平均逃避潜伏期较BC组和AC组明显延长,差异有统计学意义(P<0.05).DEACMP组凋亡指数(AI)在染毒后第1天开始逐渐升高,第7天达峰值,并保持较高水平持续到第28天,各时间点均高于BC组和AC组,差异有统计学意义(P<0.05).DEACMP组EPO蛋白的表达从染毒后的第1天开始有较明显的升高,在染毒后第3天达到峰值,第7天后开始逐渐降低,各时间点EPO表达高于BC组和AC组,差异有统计学意义(P<0.05).结论 EPO在急性一氧化碳中毒中后期表达降低、抗凋亡作用减弱可能是DEACMP发病原因之一.%Objective To observe the effect of erythropoietin(EPO)in rats with delayed encephalopathy after acute carbon monoxide poisoning (DEACMP). Methods A total of 90 male adult SD rats were randomly divided into three groups:blank control group(BC group),air control group(AC group)and DEACMP group. Time points(1,3,7,14,21 and 28 days after acute carbon monoxide poisoning)were set for measuring the changes. Pure CO were injected into the abdominal cavity of the rats from DEACMP group for several times to estab-lish DEACMP model. Rats in AC group were injected with equal volume of air by the same way. BC group were without any treatment. Morris water maze test was used to measure the cognitive behavior. The apoptosis of pyrami-dal neurons at hippocampus was measured by TUNEL. The expression of erythropoietin(EPO)in hippocampus was measured by immunohistochemistry. Results The average escaped latency of rats in DEACMP group increased after poisoning compared with rats in other two groups(P<0.05). The apoptosis of pyramidal neurons in hippocam-pus increased from day 1 after the CO poisoning. It reached the peak at day 7 and it still had a high expression at day 28. The apoptotic index in DEACMP group increased significantly compare with that of BC group and AC group (P < 0.05). The expression of EPO in hippocampus was found increased from day 1 after the CO poisoning and reached the peak at day 3. It began to reduce at day 7. The expression in DEACMP group was higher than those of other two groups (P < 0.05). Conclusions It may be one of the causes of the DEACMP that the expression of EPO decreased in the middle and late stage after CO poisoning and its anti-apoptosis was decreased.