TargetRx Atlas

MRNA basic information

  • mRNA ID:ENST00000445232
  • Gene Name:TNF
  • mRNA database:Ensembl
  • mRNA expression :down-regulated
  • mRNA Method:PCR
  • mRNA Pathway:NA
  • Evidence:validated
  • (mRNA-drug)

Drug basic information

  • Drug ID:DB00482
  • Drug Name:Celecoxib
  • Drug Method:down-regulated the gene expression

Disease basic infommation

  • Disease:lumbar spinal stenosis
  • Tissue:patients tissues

Other information

  • Title:Inhibition of COX-2 alleviates lumbar spinal stenosis-induced chronic mechanical allodynia in rats
  • Journal:International Immunopharmacology
  • Published:2019
  • PubMed ID:31306980
  • 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-α, Il-1β, 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.
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