目的 探讨粒细胞集落刺激因子（G-CSF）对急性脊髓损伤条件下神经保护作用的具体机制。方法 建立小鼠半切脊髓损伤模型。体内实验于造模成功术后第1天开始，给予G-CSF，连续3天，进行Basso-Beattie-Bresnahan (BBB)评分后处死，取脊髓组织进行免疫荧光及免疫印迹（Western blotting）检测。体外培养神经元，建立机械损伤细胞模型，进行形态学观察及缺口末端标记（TUNEL）染色。结果 G-CSF能够促进急性脊髓损伤后运动功能的修复，粒细胞集落刺激因子受体与核磷蛋白（NPM1

Objective To explore the mechanism of granulocyte-colony stimulating factor (G-CSF) on neuronal protective function in acute spinal cord model mice. Methods Hemi-section injury was produced by cutting one-half of the right lateral portions of the spinal cord. After the surgery the mouse accepted an intraperitoneal injection of recombinant human granulocyte colony-stimulating factor(rhGCSF), once a day for 3 days. Behavior of the mouse was analyzed with Basso-Beattie-Bresnahan(BBB) locomotor rating scale. The spinal cord of the mouse was then dissected and examined with histological immunofluorescence and Western blotting analysis. We established neuron mechanical injury model EM>in vitro/EM>. Morphological changes were observed and TUNEL staining was used to investigate the apoptosis. Results In the G-CSF group, improvement in hindlimb motor function was significantly greater than that in the injury group. G-CSF receptor was expressed specifically on the neurons. After treatment with G-CSF in acute spinal cord injury, nucleophosmin 1(NPMI) expression was significantly increased and apoptotic cells decreased. After treatment with NSC348884, a specific nucleophosmin inhibitor, in neuron mechanical injury model EM>in vitro/EM>, apoptotic neurons increased and the function of G-CSF on neuronal protection was decreased.Conclusion G-CSF improves motor function in acute spinal cord injury. Moreover, this protective effect may be achieved through the anti-apoptotic role of NPM 1.