• G Sakaue, M Shimaoka, T Fukuoka, T Hiroi, T Inoue, N Hashimoto, T Sakaguchi, Y Sawa, R Morishita, H Kiyono, K Noguchi, and T Mashimo.
• Department of Anesthesiology, Osaka University Medical School, 2-2 Yamada-Oka, Suita, Osaka 565-0871, Japan.
• Neuroreport. 2001 Jul 20; 12 (10): 2079-84.

AbstractPro-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.

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