• Kei Kato, Masao Koda, Hiroshi Takahashi, Tsuyoshi Sakuma, Taigo Inada, Koshiro Kamiya, Mitsutoshi Ota, Satoshi Maki, Akihiko Okawa, Kazuhisa Takahashi, Masashi Yamazaki, Masaaki Aramomi, Masayuki Hashimoto, Osamu Ikeda, Chikato Mannoji, and Takeo Furuya.
• Department of Orthopedic Surgery, Chiba University Graduate School of Medicine, Japan.
• J. Neurol. Sci. 2015 Aug 15; 355 (1-2): 79-83.

AbstractSpinal cord injury (SCI) can cause neuropathic pain (NeP), often reducing a patient's quality of life. We recently reported that granulocyte colony-stimulating factor (G-CSF) could attenuate NeP in several SCI patients. However, the mechanism of action underlying G-CSF-mediated attenuation of SCI-NeP remains to be elucidated. The purpose of the present study was to elucidate the therapeutic effect and mechanism of action of granulocyte colony-stimulating factor for SCI-induced NeP. T9 level contusive SCI was introduced to adult male Sprague Dawley rats. Three weeks after injury, rats received intraperitoneal recombinant human G-CSF (15.0 μg/kg) for 5 days. Mechanical allodynia was assessed using von Frey filaments. Immunohistochemistry and western blot analysis were performed in spinal cord lumbar enlargement samples. Testing with von Frey filaments showed significant increase in the paw withdrawal threshold in the G-CSF group compared with the vehicle group 4 weeks, 5 weeks, 6 weeks and 7 weeks after injury. Immunohistochemistry for CD11b (clone OX-42) revealed that the number of OX-42-positive activated microglia was significantly smaller in the G-CSF group than that in the vehicle rats. Western blot analysis indicated that phosphorylated-p38 mitogen-activated protein kinase (p38MAPK) and interleukin-1β expression in spinal cord lumbar enlargement were attenuated in the G-CSF-treated rats compared with that in the vehicle-treated rats. The present results demonstrate a therapeutic effect of G-CSF treatment for SCI-induced NeP, possibly through the inhibition of microglial activation and the suppression of p38MAPK phosphorylation and the upregulation of interleukin-1β.Copyright © 2015 Elsevier B.V. All rights reserved.

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