Inhibition of COX-2 alleviates lumbar spinal stenosis-induced chronic mechanical allodynia in rats

Authors
Lee, Jee YounChol, Hae YoungPark, Chan SolJang, ChangyoungLee, Kyung TaeLee, Jae YeolYoun, InchanYune, Tae Young
Issue Date
2019-10
Publisher
ELSEVIER
Citation
INTERNATIONAL IMMUNOPHARMACOLOGY, v.75
Abstract
Chronic low back pain due to lumbar spinal stenosis (LSS) is common, costly, mechanistically complex, and clinically challenging. However, the factors and mechanisms causing and mediating chronic pain induced by cauda equina compression remain unclear. Here, we examined the role of cyclooxygenase (COX)-2 in infiltrated macrophages, a key mediator of inflammation, in chronic neuropathic pain by LSS using an animal model. LSS was induced in adult male rats by cauda equina compression procedure using a silicone block within the epidural spaces of L5-L6 vertebrae. Locomotor deficit was observed after compression and mechanical allodynia was developed progressively for 4 weeks after injury. A number of macrophage were also infiltrated into the spinal parenchyma and cauda equina and COX-2 was expressed in infiltrated macrophages at 28 days after cauda equina compression. The administration of COX-2 inhibitors, celecoxib and MPO-0029, significantly alleviated LSS-induced chronic mechanical allodynia and inhibited the mRNA expression of inflammatory mediators such as tnf-alpha, Il-1 beta, il-6, and inos. Furthermore, COX-2 inhibitors significantly reduced prostaglandin E2 production. These results demonstrated the role of COX-2 in LSS-induced chronic neuropathic pain and suggest that the regulation of COX-2 can be considered as a therapeutic target to relive neuropathic pain.
Keywords
EQUINA COMPRESSION INJURY; NEUROPATHIC PAIN; MICROGLIA; EXPRESSION; MODEL; DECOMPRESSION; HYPERALGESIA; EQUINA COMPRESSION INJURY; NEUROPATHIC PAIN; MICROGLIA; EXPRESSION; MODEL; DECOMPRESSION; HYPERALGESIA; Lumbar spinal stenosis; Cauda equina; Neuropathic pain; Inflammation; Cyclooxygenase-2
ISSN
1567-5769
URI
https://pubs.kist.re.kr/handle/201004/119508
DOI
10.1016/j.intimp.2019.105738
Appears in Collections:
KIST Article > 2019
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