1Department of Orthopedics and Rehabilitation Medicine, Faculty of Medical Sciences, The University of Fukui, Fukui, Japan
2Research and Education Program for Life Science, The University of Fukui, Fukui, Japan
3Department of Orthopedic Surgery, Suzuki Orthopaedic Clinics, Toki, Gifu, Japan
4Department of Orthopedic Surgery, Yamada Orthopaedic Clinics, Hamamatsu, Shizuoka, Japan
5Victor Horsley Department of Neurosurgery, The National Hospital for Neurology and Neurosurgery, Queen Square, London, UK
International Journal of Clinical and Experimental Neurology.
2015,
Vol. 3 No. 2, 26-31
DOI: 10.12691/ijcen-3-2-1
Copyright © 2015 Science and Education PublishingCite this paper: Shigeru Kobayashi, Yoshihiko Suzuki, Syuichi Yamada, Naji Al-Khudairi, Adam Meir. Cyclooxygenase Expression in Canines Following Peripheral Nerve Injury.
International Journal of Clinical and Experimental Neurology. 2015; 3(2):26-31. doi: 10.12691/ijcen-3-2-1.
Correspondence to: Shigeru Kobayashi, Department of Orthopedics and Rehabilitation Medicine, Faculty of Medical Sciences, The University of Fukui, Fukui, Japan. Email:
kshigeru@u-fukui.ac.jpAbstract
In order to investigate the mechanism of neurogenic pain, this study used a median nerve compression model in dogs. The nerve was compressed with a clip for three weeks. Immunohistochemistry was done by the avidin-biotin-peroxidase complex method to observe the changes of T cells (CD45) and macrophages (Mac-1) after compression. Antibodies against cyclooxygenase (COX)-1 and 2 were used to examine the localization and changes of these mediators caused by nerve compression. In control animals, resident T cells were detected, but there were no macrophages. COX-2 was positive in the Schwann cells and vascular endothelial cells, while COX-1 was detected in the vascular endothelial cells. After nerve compression, numerous T cells and macrophages appeared among the demyelinized nerve fibers. The macrophages were positive for COX-2. COX-2 may be deeply involved in neuritis arising from mechanical compression, and this mediator seems to be important in the manifestation of neurogenic pain.
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