Antiapoptotic Effect of Granulocyte-Colony Stimulating Factor After Peripheral Nerve Trauma

World Neurosurg. 2019 Sep:129:e6-e15. doi: 10.1016/j.wneu.2019.04.059. Epub 2019 Apr 11.

Abstract

Background: Granulocyte-colony stimulating factor (G-CSF) has been observed to have direct protective effects on neurons after stroke in experimental models and in humans. In the present study, the antiapoptotic effects of G-CSF on spinal α-motoneurons after inducement of peripheral sciatic nerve lesions were evaluated in a rat model.

Methods: Of 48 rats, 24 were treated with G-CSF and 24 were treated with glucose 5% solution (control group). The spinal cord of 6 rats in each group were removed at days 1, 4, 7, and 14. The α-motoneurons of spinal cord section L4-L6 were counted and investigated for the expression of choline acetyltransferase (ChAT), G-CSF receptor (G-CSFR), and Bcl-2 and Bax proteins. Additionally, α-motoneuron fluorescence double staining was performed for ChAT/Bcl-2, ChAT/Bax, and ChAT/G-CSFR.

Results: Without G-CSF treatment, the number of ChAT-positive α-motoneurons on the lesion side was significantly decreased (P < 0.001). The number of α-motoneurons with Bcl-2 and G-CSFR positivity on the lesion side was significantly decreased (P < 0.05). In contrast, the number of α-motoneurons with Bax positivity was significantly greater (P < 0.05). After G-CSF treatment, the differences in the number of α-motoneurons on the 2 sides were not statistically significant. Fluorescence double staining of α-motoneurons was positive for ChAT/Bcl-2, ChAT/Bax, and ChAT/G-CSFR.

Conclusion: The results indicated that G-CSF has neuroprotective properties in spinal α-motoneurons and contributes to antiapoptotic effects after peripheral nerve lesions. The relevance of G-CSF, its precise mode of action, and the effect of these findings in clinical situations remains to be elucidated and require examination in further studies.

Keywords: G-CSF; Nerve regeneration; Peripheral nerve lesion; Traumatic nerve injury; Waterjet dissection.

MeSH terms

  • Animals
  • Apoptosis / drug effects*
  • Granulocyte Colony-Stimulating Factor / pharmacology*
  • Male
  • Motor Neurons / drug effects*
  • Motor Neurons / pathology
  • Neuroprotective Agents / pharmacology*
  • Peripheral Nerve Injuries / pathology*
  • Rats
  • Rats, Sprague-Dawley

Substances

  • Neuroprotective Agents
  • Granulocyte Colony-Stimulating Factor