Therapy of neuropathic pain by using a gene-based approach of NF-κB decoy

促炎细胞因子已被证明与神经损伤后神经病理性疼痛的发生、持续和严重程度有关。核转录因子-kappaB(NF-κB)在调节促炎细胞因子基因表达中起着关键作用。为了阐明NF-κB在神经病理性疼痛发病机制中的作用，我们采用基于基因的方法检测了激活的NF-κB是否通过炎性介质的表达影响了疼痛行为。神经损伤区单次神经内注射，NF-κB诱骗物可明显减轻持续2周的热痛觉过敏，并抑制神经损伤区炎性细胞因子、诱导型一氧化氮合酶和黏附分子的表达。这一发现表明，神经周围炎性级联反应，包括核因子-κB，与神经病理性疼痛的发病机制有关

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-κB), palys a pivotal role in regulating pro-inflammatory cytokine gene expression. To elucidate the role of NF-κB in the pathogenesis of neuropathic pain, using a gene-based approach of NF-κB decoy, we tested whether the activated NF-κB affected pain behavior via the expression of inflammatory mediators. Single endoneurial injections' of, NF-κB 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-κB, is involved in the pathogenesis of neuropathic pain