Inhibiting IκB kinase-β downregulates inflammatory cytokines in injured discs and neuropeptides in dorsal root ganglia innervating injured discs in rats.

摘要: STUDY DESIGN Quantitative and immunohistological analysis of the efficacy an IκB kinase-β (IKKβ) inhibitor in injured intervertebral disc (IVD) model. OBJECTIVE To elucidate IKKβ on inflammatory cytokine levels IVDs or neuropeptide dorsal root ganglia (DRG) neurons innervating rats. SUMMARY OF BACKGROUND DATA Multiple studies have suggested that upregulation cytokines damaged causes discogenic low back pain. The blocking individual is limited; however, stimuli often require to activate nuclear factor-k B. METHODS Sprague-Dawley rats were divided into 3 groups: sham, saline (disc-injury plus saline), anti-IKKβ). induce injury, repeatedly punctured.Experiment 1: Four, 7, 14 days postinjury, coccygeal (Co) 5/6, Co6/7, Co7/8 resected tumor necrosis factor-α, interleukin (IL)-1β, IL-6 quantified by enzyme-linked immunosorbent assay. Experiment 2: neurotracer Fluoro-Gold was injected L5-L6 uninjured sham group detect DRG neurons. One week postsurgery, L1-L6 DRGs immunolabeled with calcitonin gene-related peptide. proportions Fluoro-Gold-labeled peptide-immunoreactive assessed. RESULTS IVD factor-α (through 2 wk), IL-1β (at 4 d), d) significantly higher than group, lower (P < 0.05). percentage CONCLUSION Injury-induced within increased neuropeptides can be suppressed inhibiting IKKβ. LEVEL EVIDENCE N/A.