ArticleFrontiers in aging neuroscience2026
Needle-warming moxibustion alleviates pain in rats with cervical spondylotic radiculopathy by modulating the NF-κB/ROS/NLRP3 pathway.
Article in Frontiers in aging neuroscience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Aim: This study investigates the effects of needle-warming moxibustion (NWM) on cervical spondylotic radiculopathy (CSR) by regulating the activation of the nuclear factor-kappa B (NF-κB) pathway. Methods: A CSR rat model was prepared using the fish wire extrusion method and administered postoperative treatment with NWM or injection with MitoTEMPO, with pain pressure threshold and mechanical pain threshold evaluated. Limb spasm pain-caused gait disorders were assessed using the Kawakami method. Pain mediators [Substance P (SP), Prostaglandin E2 (PGE2), and Neuropeptide Y (NPY)] and inflammatory cytokines, ROS levels, spinal cord tissue damage and positive neurons were assessed by ELISA, DHE, HE, and TUNEL staining, respectively. Serum samples from 100 CSR patients treated with NWM were collected before and after treatment. Serum inflammatory factors were determined by ELISA. Visual Analogue Scale (VAS) scores and Neck Disability Index (NDI) scores were assessed before and after treatment for CSR patients. Results: NWM increased pain thresholds and decreased SP, PGE2, and NPY protein expression and gait scores in CSR rats, indicating that NWM alleviated pain and improved motor function in CSR rats. NWM reduced inflammatory factor levels and TUNEL-positive neurons. NWM reduced ROS levels and the NLRP3 pyroptosis pathway and the NF-κB signaling axis-related protein expression in damaged tissue of CSR rats. NWM treatment reduced serum inflammatory factors and VAS and NDI scores in CSR patients. Improvements in NDI scores were positively correlated with reduced levels of IL-1β, TNF- Conclusion: NWM attenuates CSR by regulating the activation of the NF-κB pathway, reducing ROS, affecting the activation of the NLRP3 inflammasome, and inhibiting mitochondrial dysfunction.
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