摘要目的 探讨急性一氧化碳中毒(acute carbon monoxide poisoning,ACOP)对大鼠大脑少突胶质前体细胞(oligodendrocyte precursor cells,OPCs)分化功能的影响.方法 利用分次腹腔注射制作ACOP大鼠模型,60只SD大鼠按随机数字表法选取45只进行染毒,造模结束后从存活大鼠中随机选取15只作为ACOP组,对照组15只大鼠按同样方案注射空气.分别在造模成功后1、3、7、14 d和30 d时取大鼠脑组织,采用免疫荧光组织化学法分别检测大脑皮质和海马NG2和CC1阳性细胞数目.结果 (1)与对照组相比,ACOP组大鼠脑内NG2阳性细胞胞体形态不规则、皱缩,且突起数量明显减少;(2)与对照组相比,处理后1d和3d时ACOP组大鼠大脑皮层内NG2阳性细胞数目明显较多(P＜0.05);7d时ACOP组NG2阳性细胞数目开始减少(P＜0.05),14 d和30 d时减少更加明显(P＜0.01).CC1阳性细胞数目处理后第3天开始减少(P＜0.05),7d时最明显(P＜0.01),14 d和30 d时CC1阳性细胞数目亦较对照组少(P＜0.05).但与14 d相比,30 d时ACOP组大鼠脑内皮层CC1阳性细胞数目增加约50％.(3)与对照组相比,处理后1d时ACOP组大鼠大脑海马内NG2阳性细胞数目明显较多(P＜0.01);3d时NG2阳性细胞数目稍减少(P＞0.05),7、14 d和30 d时明显减少(P＜0.01).ACOP组大鼠大脑海马内CC1阳性细胞数目处理后1、3、7、14 d和30 d时均较对照组减少(P＜0.05).结论 大鼠ACOP后OPCs和少突胶质细胞(oligodendrocytes,OLs)均会受到不同程度的损伤,同时可能会调动机体自我修复能力,诱导OPCs增殖、分化成为成熟的OLs,从而实现髓鞘损伤修复.

abstractsObjective To explore the effects of acute carbon monoxide poisoning (ACOP) on the differentiation of oligodendrocyte precursors in the brain of rats.Methods ACOP rat model was developed by intraperitoneal injection of CO to 45 SD rats from the samples of 60 rats and selected 15 rats from the survival rats as the ACOP group,and the remaining 15 rats were designated as the control group,which were injected air according to the same treatment scheme.Following development of the model,brain tissue samples of the rats were collected at day 1,3,7,14 and 30.hnmunofluorescence histochemistry was used to detect the number of NG2 and CC1 positive cells in the cortex and hippocampus.Results (1) As compared with the control group,the NG2 positive cells in the ACOP group displayed irregular shape,with shrinkage and a decreased number.(2) Following treatment at day 1 and 3,the number of NG2 positive cells in cerebral cortex of the ACOP group was significantly increased(P ＜ 0.05).However,it began to decrease at day 7 (P ＜ 0.05),and the decreasing trend became more prominent at day 14 and 30 (P ＜ 0.01).The number of CC1 positive ceils began to decrease at day 3 (P ＜ 0.05),and the decreasing trend became more prominent at day 7 (P ＜ 0.01).And at day 14 and 30,the number of CC1 positive cells was smaller as compared with that of the control group(P ＜ 0.05).However,the number of CC1 positive cells in the cerebral cortex of the ACOP group at day 30 was increased by about 50％,when compared with that at day 14.(3)As compared with the control group,the number of NG2 positive cells in the hippocampus of the ACOP group was obviously increased at day 1 after treatment(P ＜ 0.01).However,the decreasing trend became less prominent at day 7,14 and 30(P ＜0.01).The number of CC1 positive cells in the hippocampus of the ACOP group was decreased as compared with that of the control group at day 1,3,7,14,30 (P ＜ 0.05).Conclusions Following ACOP,oligodendrocyte precursors (OPCs) and oligodendrocytes (OLs) in the brain of rats were damaged to a certain extent,the mechanism might be the mobilization of self-repair,the induction of OPCs proliferation and differentiation of mature OLs,and as a consequence,the repair of damaged myelin was achieved.