Department of Surgery (Division of Neurosurgery), College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Spine (Phila Pa 1976). 2012 Jan 1;37(1):10-7. doi: 10.1097/BRS.0b013e31823b0440.
We used a severe contusive spinal cord injury (SCI) model and electrophysiologic, motor functional, immunohistochemical, and electron microscopic examinations to analyze the neuroprotective effects of delayed granulocyte colony-stimulating factor (G-CSF) treatment.
To determine the neuroprotective effects of delayed G-CSF treatment using multimodality evaluations after severe contusive SCI in rats.
Despite some reports that G-CSF treatment in the acute stage of different central nervous system injury models was neuroprotective, it has not been determined whether delayed G-CSF treatment can promote neural recovery in severe contusive SCI.
Rats with severe contusive SCI were divided into 2 groups: G-CSF group rats were given serial subcutaneous injections of G-CSF, and control group rats (controls) were given only saline injections on postcontusion days 9 to 13. Using the Basso-Beattie-Bresnahan scale and cortical somatosensory evoked potentials, we recorded functional evaluations weekly. The spinal cords were harvested for protein and immunohistochemical analysis, and for electron microscopy examination.
The preserved spinal cord area was larger in G-CSF group rats than in control group rats. Both sensory and motor functions improved after G-CSF treatment. Detachment and disruption of the myelin sheets in the myelinated axons were significantly decreased, and axons sprouted and regenerated. There were fewer microglia and macrophages in the G-CSF group than in the control group. The levels of brain-derived neurotrophic factor were comparable between the 2 groups.
Delayed G-CSF treatment at the subacute stage of severe contusive SCI promoted spinal cord preservation and improved functional outcomes. The mechanism of G-CSF's protection may be related in part to attenuating the infiltration of microglia and macrophages.
我们使用严重创伤性脊髓损伤（SCI）模型以及电生理、运动功能、免疫组织化学和电子显微镜检查，分析延迟粒细胞集落刺激因子（G-CSF）治疗的神经保护作用。
通过对大鼠严重创伤性 SCI 后的多模态评估，确定延迟 G-CSF 治疗的神经保护作用。
尽管有一些报告称 G-CSF 治疗不同中枢神经系统损伤模型的急性期具有神经保护作用，但尚未确定延迟 G-CSF 治疗是否能促进严重创伤性 SCI 中的神经恢复。
将严重创伤性 SCI 大鼠分为 2 组：G-CSF 组大鼠给予连续皮下注射 G-CSF，对照组大鼠（对照组）仅在挫伤后第 9 至 13 天给予生理盐水注射。使用 Basso-Beattie-Bresnahan 量表和皮质体感诱发电位每周进行功能评估。收获脊髓进行蛋白质和免疫组织化学分析，并进行电子显微镜检查。
G-CSF 组大鼠保留的脊髓面积大于对照组大鼠。G-CSF 治疗后感觉和运动功能均有所改善。髓鞘轴突中的髓鞘片分离和破坏明显减少，轴突发芽和再生。G-CSF 组的小胶质细胞和巨噬细胞比对照组少。两组脑源性神经营养因子水平相当。
严重创伤性 SCI 亚急性期的延迟 G-CSF 治疗促进了脊髓的保存，并改善了功能结果。G-CSF 保护的机制部分可能与减轻小胶质细胞和巨噬细胞的浸润有关。
