急性一氧化碳中毒对大鼠少突胶质细胞前体细胞活性及增殖能力的影响  

Effects of acute carbon monoxide poisoning on the activity and proliferation of oligodendrocyte precursors in rats

作　　者：郭大志[1] 冯园[1] 潘树义[1] Guo Dazhi;Feng Yuan;Pan Shuyi(Hyperbaric Oxygen Center, Navy General Hospital of CPLA, Beijing 100048, China)

机构地区：[1]海军总医院高压氧中心,北京100048

出　　处：《中华航海医学与高气压医学杂志》2018年第6期337-341,共5页Chinese Journal of Nautical Medicine and Hyperbaric Medicine

基　　金：北京市自然科学基金资助项目(7153175).

摘　　要：目的探讨急性一氧化碳中毒(acute carbon monoxide poisoning,ACOP)对大鼠少突胶质细胞前体细胞( oligodendrocyte precursors, OPCs)活性及增殖能力的影响。方法选取实验用SD新生大鼠24只,取脑后,采用差速贴壁法体外纯化和培养大鼠OPCs完成后,按照数字表法随机分成对照组和ACOP组,每组12只。ACOP组将OPCs放置于密闭容器内,根据体积比注入1%的CO,处理6、24和48 h后分别利用免疫荧光细胞化学法观察OPCs形态和数量,MTT法检测OPCs活性,Brdu染色检测OPCs增殖情况。结果与对照组相比,ACOP组OPCs胞体呈扁平状、皱缩,突起数目减少、变短,且数量减少;ACOP组6 h时OPCs活性无明显改变,24、48 h时细胞活性明显降低(P<0.05),其中48 h细胞活力降低最显著;ACOP组6 h时OPCs的Brdu阳性率明显升高(P<0.05),24 h时2组无明显差异(P>0.05),48 h时Brdu阳性率较对照组显著降低(P<0.05)。结论ACOP对OPCs造成不可逆性损伤,显著影响其活性和增殖能力,了解其作用机制对一氧化碳中毒迟发性脑病(delayed encephalopathy after acute carbon monoxide poisoning, DEACMP)及寻找其更有效的治疗方法具有重要意义。Objective To explore the effects of acute carbon monoxide poisoning (ACOP) on the activity and proliferation of oligodendrocyte precursors (OPCs) in rats. Methods OPCs were purified and cultured by differential adherence method in vitro, and the exogenous carbon monoxide was used for direct treatment of OPCs in vitro for the establishment of OPCs model of ACOP. The morphology and quantity of OPCs were observed by immunofluorescence staining, and the activity was detected by MTT method. The proliferation of OPCs was detected by Brdu staining. Results Compared with that of the control group, OPCs body in the ACOP group was flat and shrinking, the number of dendrites was reduced and its length became shorter. There were no obvious changes in the viability of OPCs at hour 6 in the ACOP group, however at hour 24 and 48, there were remarkable changes in the viability of OPCs, with its change at hour 48 decreasing most significantly (P<0.05). The Brdu positive rate of OPCs in the ACOP group increased significantly at hour 6 (P<0.05), however, at hour 24, no significant differences could be seen when comparisons were made between the 2 groups (P>0.05). The Brdu positive rate of OPCs in the ACOP group decreased significantly as compared with that of the control group (P<0.05). Conclusion ACOP could cause irreversible damage to OPCs and significantly affect its activity and rate of proliferation. Deep understanding of the mechanism of ACOP was great importance to get an inmate knowledge of delayed encephalopathy after acute carbon monoxide poisoning(DEACMP)and to seek more effective therapeutic method for the disorder.

关 键 词：一氧化碳中毒 少突胶质细胞前体细胞 细胞活性 增殖 

分 类 号：R595.1[医药卫生—内科学]