目的  通过对大脑皮层Sox10细胞进行谱系示踪，探讨少突胶质谱系细胞在神经损伤后的分化。 方法  分别选用C57BL/6小鼠和Sox10-CreERT2/红色荧光蛋白（RFP）模型小鼠为研究对象。Sox10-CreERT2/RFP模型小鼠由Sox10-CreERT2和Ai9杂交后获得8周龄F1代小鼠（n =16），随机分为对照组（n =4）和7 d（n =4）、14 d（n =4）、30 d他莫昔芬（TAM）饲料组（n =4），用他莫昔芬诱导RFP。对照组用他莫昔芬溶于葵花籽油后灌胃（40 mg/kg），每天1次，连续3 d，于4 d后获取脑组织；饲料组用他莫昔芬饲料喂食诱导RFP，分别于7 d、14 d和30 d后获取脑组织。采用免疫荧光染色检测神经元核抗原（NeuN）、微管相关蛋白2（MAP2）、磷酸化组蛋白2AX（γ-H2AX）、分化簇13（CD13）、γ-氨基丁酸（GABA）、胶质纤维酸性蛋白（GFAP）、分化簇11b（CD11b）、囊泡型谷氨酸转运蛋白2（VGLUT2）和结肠腺瘤息肉易感蛋白（APC，CC-1）在各组小鼠大脑中的表达情况，统计阳性细胞数并计算比例。选用8周龄雄性C57BL/6小鼠随机分为野生型（WT）组（n =4）和WT+TAM组（n =4），分别使用普通饲料和他莫昔芬饲料喂食30 d后获取脑组织；免疫荧光双标染色检测γ-H2AX 阳性神经元在两组小鼠大脑皮层中的表达情况。 结果  在对照组、7 d、14 d和30 d饲料组大脑皮层出现RFP+周细胞占全部RFP+细胞比例分别为: (0.8±0.1)%、(2.7±0.1)%、(3.2±0.1)%和 (4.0±0.1)%，7 d饲料组CC-1+RFP+成熟的少突胶质细胞（OL）比例为(51.2±0.7)%。他莫昔芬饲料喂食14 d和30 d组皮层的RFP阳性神经元比例为 (0.7±0.1)%及 (1.5±0.1)%，而在对照组和7 d饲料组未发现转化为RFP阳性神经元。在7 d或30 d饲料组的皮层中，RFP细胞不表达GFAP或CD11b。WT组和WT+TAM组中出现大面积γ-H2AX阳性神经元。 结论  长期给药他莫昔芬促进Sox10细胞分化为周细胞和神经元，进一步研究少突胶质谱系细胞对神经血管单元修复机制可能有助于理解AD的发病原因。 

Objective To investigate the differentiation of oligodendrocyte precursor cells after neural injury utilizing Sox10 cell lineage tracing in the cortical tissue. Methods  C57BL/6 mice and Sox10-CreERT2/red fluorescent protein(RFP) model mice were used in the current study. The Sox10-CreERT2/RFP model mice generated by crossing Sox10-CreERT2 and Ai9 were 8-week-old F1 mice (n =16), which were randomly divided into control group (n =4) and 7 days (n =4), 14 days (n =4), and 30 days feed groups (n =4). Tamoxifen(TAM) was used to induce the expression of RFP. The control group received tamoxifen dissolved in sunflower seed oil by gavage (40 mg/kg once daily for three consecutive days) and the brain tissues were obtained after 4 days. The feed group mice were fed with tamoxifen-containing feed to induce RFP expression, and the brain tissues were obtained after 7, 14, and 30 days, respectively. Immunofluorescent staining was performed to detect the expressions of neuronal nuclei (NeuN), microtubuleassociated protein 2 (MAP2), phosphorylated histone 2AX (γ-H2AX), cluster of differentiation 13 (CD13), γaminobutyric acid (GABA), glial fibrillary acidic protein (GFAP), cluster of differentiation 11b (CD11b), vesicular glutamate transporter 2 (VGLUT2), and adenomatous polyposis coli (APC, CC-1) in the brains of each group mice. The number of positive cells was counted, and the proportion was calculated. Eight-week-old male C57BL/6 mice were randomly divided into wild type(WT) group (n =4) and WT+TAM group (n =4). They were fed with regular feed and tamoxifencontaining feed for 30 days, respectively, and then brain tissues were obtained. Immunofluorescent double-labeling was used to detect the expressions of γ-H2AX positive neurons in the cortex of mice in both groups.   Results  In the control group, feed 7 days,14 days, and 30 days groups, the proportions of RFP⁺ pericytes among all RFP⁺ cells in the cortical tissue were (0.8±0.1)%, (2.7±0.1)%, (3.2±0.1)%, (4.0 ±0.1)%, respectively, and the proportion of mature oligodendrocytes (CC-1⁺ RFP⁺) in the feed 7 days group was (51.2±0.7)%. The proportions of RFPpositive neurons in the cortex after 14 and 30 days of tamoxifen feed were (0.7±0.1)% and (1.5±0.1)%, respectively, while no conversion to RFP-positive neurons was observed in the gavage group and 7 days feed group. RFP cells in the cortex of the 7 days or 30 days feed group did not express GFAP or CD11b. Extensive γ-H2AX⁺ NeuN⁺ staining was observed in the WT group and WT+TAM group. Conclusion  Long-term administration of tamoxifen can promote the differentiation of Sox10 cells into pericytes and neurons. Further investigation into the role of OPC in the neurovascular unit repair mechanism may contribute to a better understanding of the pathogenesis underlying AD.