Acupuncture and Moxibustion Therapy Attenuates Inflammation in CCI-Induced Sciatica by Inhibiting the NF-κB Pathway

Objectives: To investigate the analgesic and anti-inflammatory effects of an integrated acupuncture-moxibustion regimen in a rat model of chronic constriction injury (CCI)induced sciatica, with particular emphasis on NF-κB p65 expression and nuclear translocation as activation-related indicators of NF-κB-associated neuroimmune signaling.Methods: A rat CCI model was established and randomly allocated into four experimental groups: sham surgery (Sham), untreated CCI (CCI), active drug comparator (Drug), and acupuncture-moxibustion therapy (Acu).Pain-related behavioral alterations were evaluated using thermal withdrawal latency (TWL) and mechanical withdrawal threshold (MWT) assessments.Histopathological alterations in the sciatic nerve and spinal cord were examined using hematoxylin-eosin staining.The expression of proinflammatory cytokines, including IL-1β, IL-6, IL-8, and TNF-α, was quantified by quantitative real-time PCR and enzyme-linked immunosorbent assay (ELISA).NF-κB activation-related changes were further evaluated by immunohistochemistry and immunofluorescence analyses focusing on NF-κB p65 expression and nuclear localization.Results: Compared with the CCI group, rats receiving acupuncture-moxibustion therapy demonstrated significant recovery of TWL and MWT values, indicating attenuation of neuropathic pain hypersensitivity.Histological analyses revealed substantial preservation of sciatic nerve and spinal cord architecture following treatment.RT-qPCR and ELISA findings showed marked reductions in proinflammatory cytokine expression and circulating inflammatory mediator levels in the Acu group.Furthermore, immunohistochemical and immunofluorescence analyses demonstrated significant suppression of NF-κB p65 expression and reduced nuclear translocation following acupuncture-moxibustion intervention.Conclusion: Acupuncture-moxibustion therapy effectively ameliorated CCI-induced sciatica and was associated with suppression of proinflammatory cytokine production and attenuation of NF-κB-associated inflammatory signaling, providing mechanistic support for integrative non-pharmacological strategies in neuropathic pain management.