TNF-α expression, not iNOS expression, is correlated with NF-κB activation in the spinal cord of rats following peripheral nerve injury
Previous studies have shown that pro-inflammatory cytokines were involved in the genesis and persistence of neuropathic pain. Nuclear factor kappa B (NF-κB) plays a crucial role in regulating proinflammatory cytokine gene expression. In this study, we examined the hypothesis that NF-κB would regulate the expression of spinal tumor necrosis factor α (TNF-α) and inducible nitric oxide synthase (iNOS) following chronic constriction nerve injury (CCI) in rats. CCI induced a significant upregulation of NF-κB in the ipsilateral spinal cord on postoperative Day 7 as revealed by Western blot, immunohistochemistry and real time polymerase chain reaction (real time-PCR). Moreover, TNF-α mRNA expression was markedly upregulated by CCI, whereas only a low level of iNOS mRNA was detected in the ipsilateral spinal cord. The immunohistochemical data indicated a pattern of colocalization between NF-κB and TNF-α within spinal cord dorsal horn. These results show that NF-κB activation is correlated with TNF-α expression, but not iNOS expression, in the spinal cord after peripheral nerve injury.
Key words: Neuropathic pain, chronic constriction nerve injury, NF-κB; TNF-α, iNOS.