目的：通过制备急性一氧化碳中毒（acute carbon monoxide poisoning ，ACOP）大鼠模型，观察大鼠中毒后中枢神经系统髓鞘改变，以及髓鞘标志物髓鞘碱性蛋白（myelin basic protein ，MBP）和少突胶质前体细胞（oligoden‐drocyte precursor cells ，OPCs）特异性细胞标志物硫酸软骨素蛋白多糖 NG2在中毒后表达的变化，为研究 ACOP后中枢神经系统髓鞘脱失的机制提供实验依据。方法：24只雄性健康SD大鼠，随机分为对照组和染毒组各12只。染毒组利用分次腹腔注射CO制作急性中毒模型，对照组注射空气。于造模后1d、3d取材，采用免疫组织化学染色和Western Blot方法检测中毒后中枢神经系统髓鞘的损伤和MBP、NG2表达的变化。结果：免疫组织化学染色结果显示，与对照组比较，染毒组染毒1d后MBP、NG2表达即减少，3d时进一步降低（P＜0．05）；Western Blot结果显示，染毒组染毒1d后MBP、NG2表达即减少，3d时进一步降低（P＜0．05）。结论：ACOP后大鼠发生中枢神经系统脱髓鞘以及OPCs损伤。%Objective:To observe the changes in myelin and expression of myelin basic protein (MBP) and NG2 in the brain tissue of rats through the establishment of the acute carbon monoxide poisoning (ACOP) model ,and to provide experimental evidence for the mechanism of demyelination of the central nervous system after ACOP .Meth‐ods:Twenty‐four male rats were divided into the control group (n=12) and the intoxication group (n=12) random‐ly .Animals in the intoxication group were intraperitoneally injected with pure CO repeatedly ,and those in the con‐trol group with air by the same protocol .The brain tissues were taken from the animals of the two groups at 1st and 3rd day after the establishment of the model .Changes in myelin were observed by immunohistochemical staining , and the expression of MBP and NG2 was detected using immunohistochemistry and Western blot .Results:Immuno‐histochemistry demonstrated that the expression levels of MBP and NG 2 began to decrease at 1st day after ACOP , and there was statistically significant difference in the integral optical density (IOD) level of MBP and NG2 as com‐pared with the control group at 3rd day after ACOP (P<0 .05) .Results of Western blot showed that as compared with the control group ,the expression levels of MBP and NG2 were decreased at 1st day after ACOP ,and decreased further at 3rd day (P<0 .05) .Conclusion:Demyelination and damage of oligodendrocyte precursor cells occurred in the brain tissue of rats after ACOP .
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