NF-kappa B decoy suppresses cytokine expression and thermal hyperalgesia in a rat neuropathic pain model.

Abstract

Pro-inflammatory cytokines have been shown to be involved in the genesis, persistence, and severity of neuropathic pain following nerve injury. The transcription factor, nuclear factor-kappa B (NF-kappaB), plays a pivotal role in regulating pro-inflammatory cytokine gene expression. To elucidate the role of NF-kappaB in the pathogenesis of neuropathic pain, using a gene-based approach of NF-kappaB decoy, we tested whether the activated NF-kappaB affected pain behavior via the expression of inflammatory mediators. Single endoneurial injections of NF-kappaB decoy, at the site of nerve lesion, significantly alleviated thermal hyperalgesia for up to 2 weeks and suppressed the expression of mRNA of the inflammatory cytokines, iNOS, and adhesion molecules at the site of nerve injury. This finding suggests that a perineural inflammatory cascade, that involves NF-kappaB, is involved in the pathogenesis of neuropathic pain.

• Authors: G Sakaue, M Shimaoka, T Fukuoka, T Hiroi, T Inoue, N Hashimoto, T Sakaguchi, Y Sawa, R Morishita, H Kiyono, K Noguchi, T Mashimo
• Journal: Neuroreport (Neuroreport) Vol. 12 Issue 10 Pg. 2079-84 (Jul 20 2001) ISSN: 0959-4965 [Print] England
• PMID: 11447311 (Publication Type: Journal Article)

Chemical References

• Cell Adhesion Molecules
• Cytokines
• NF-kappa B
• RNA, Messenger
• Nitric Oxide Synthase
• Nitric Oxide Synthase Type II
• Nos2 protein, rat

Topics

• Animals
• Cell Adhesion Molecules
• Cytokines (metabolism)
• Disease Models, Animal
• Hot Temperature
• Hyperalgesia (drug therapy, metabolism)
• Male
• NF-kappa B (metabolism, pharmacology, therapeutic use)
• Neuralgia (drug therapy, metabolism)
• Nitric Oxide Synthase (metabolism)
• Nitric Oxide Synthase Type II
• RNA, Messenger (drug effects, metabolism)
• Rats
• Rats, Sprague-Dawley
• Spinal Nerves (drug effects, metabolism)