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[目的] 体外条件下研究CXCL12/CXCR4介导大鼠少突胶质前体细胞(oligodendrocyte precursor cells,OPCs)髓鞘化的作用及影响.[方法]振荡分离、差速贴壁和免疫细胞化学技术分离、培养、鉴定OPCs;Western blotting检测在不同浓度CXCL12(0、5、10、20 ng/ml)作用下,OPCs髓磷脂碱性蛋白(MBP)和髓鞘脂蛋白(PLP)的表达;CXCR4siRNA干扰CXCR4蛋白表达、LY294002抑制AKT通路活性、U0126抑制ERK通路活性,利用Western blotting检测在20ng/ml CXCL12作用下OPCs髓鞘形成相关蛋白MBP和PLP的表达,并用免疫荧光标记MBP和PLP.[结果] 随着细胞外CXCL12的浓度升高,CXCL12能够明显促进OPCs髓鞘形成相关蛋白MBP和PLP的表达.与0 ng/ml相比,CXCL12在20 ng/ml作用后,OPCs髓鞘形成相关蛋白MBP和PLP蛋白表达增加最明显(P＜0.05);干扰CXCR4蛋白表达,抑制AKT、ERK通路活性,OPCs髓鞘形成相关蛋白MBP和PLP蛋白表达受到抑制(P＜0.05).[结论] 体外条件CXCL12/CXCR4对大鼠少突胶质前体细胞参与轴突髓鞘化有促进作用,并且能够通过ERK和PI3K/AKT信号通路对髓鞘形成相关蛋白MBP和PLP蛋白表达进行调控.“,”[Objective] To study the regulatory mechanism and the promotion effect of CXCL12/CXCR4 on the myelination of rat oligodendrocyte precursor cells (OPCs) in vitro.[Method] OPCs were separated by the centrifuge and distinguished by morphological and immunocytochemical methods.The effect of different concentrations of CXCL12 (0,5,10,20 ng/ml) on OPCs myelin basic protein (MBP) and proteolipid protein (PLP) was detected by western blotting.Additionally,CXCR4 expression inhibited by CXCR4 siRNA,AKT pathway blocked by LY294002,and the ERK1/2 pathway blocked by U0126 were assessed.Furthermore,at the condition of 20 ng/mL CXCL12,OPCs myelination correlative protein MBP and PLP were detected by western blotting and immunofluorescence labelling.[Result] With the increasing of concentration,CXCL12 obviously promoted the expression of OPCs myelination correlative protein MBP and PLP.Compared with 0 ng/ml,expression of MBP and PLP increased most obviously at 20ng/ml CXCL12 condition,the difference had statistical significance (P＜0.05).As AKT and ERK1/2 pathway was restrained after CXCR4 expression,OPCs myelination had been blocked or restrained,associated with the decreasing of MBP and PLP expression,which revealed a significant difference (P＜0.05).[Conclusion] In vitro,CXCL12 / CXCR4 can regulate OPCs myelination via the AKT and ERK1/2 pathway,and promote the expression of MBP and PLP.