Open Access Peer-reviewed

Cyclooxygenase Expression in Canines Following Peripheral Nerve Injury

Shigeru Kobayashi1, 2,, Yoshihiko Suzuki3, Syuichi Yamada4, Naji Al-Khudairi5, Adam Meir5

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, 3(2), 26-31. DOI: 10.12691/ijcen-3-2-1
Published online: August 25, 2017

Abstract

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.

Keywords:

peripheral nerve, wallerian degeneration, macrophage, cyclooxigenase, entrapment neuropathy
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