• Xiangnan Li, Haiqin Yang, Qing Ouyang, Fangting Liu, Jian Li, Zhenghua Xiang, and Hongbin Yuan.
• *Department of Anesthesiology, Changzheng Hospital, the Second Military Medical University, Shanghai, 200003, China; Department of Anesthesiology, the Third People's Hospital of Yancheng, Yancheng, 224001, China;
• Pain Med. 2016 May 1; 17 (5): 803-12.

ObjectiveThere is some evidence implicating receptor for advanced glycation end products (RAGE) signaling in the pathogenesis of neuropathic pain (NP). The objective was to investigate whether RAGE signaling in the dorsal root ganglion (DRG) might contribute to NP following peripheral nerve injury.DesignExperimental study before and after spinal nerve ligation (SNL) surgery.SettingCaged in a controlled environment.SubjectsMale Sprague-Dawley rats.MethodsA SNL rat model of NP was used. Mechanical hyperalgesia was measured by the paw withdrawal threshold (PWT) to mechanical stimuli (1.4-15 g). Protein expressions of RAGE (immunofluorescence and western blotting), glial fibrillary acidic protein (GFAP; satellite glial cell [SGC] activation marker), IL-1β (ELISA), TNF-α (ELISA), and NF-κB (western blotting) in the DRG were determined. RAGE signaling was inhibited by intrathecal injection of anti-RAGE antibody.ResultsAfter 7 days, SNL surgery reduced the PWT and upregulated the protein expression of RAGE, GFAP, NF-κB, TNF-α, and IL-1β. Intrathecal injection of RAGE-neutralizing antibody attenuated the SNL-induced mechanical hyperalgesia, activation of SGCs, and upregulation of NF-κB, TNF-α, and IL-1β in the DRG.ConclusionRAGE signaling may contribute to the pain hypersensitivity observed in the rat SNL model of NP. Although the precise mechanism remains to be established, NF-κB, TNF-α, and IL-1β likely play a role, together with the activation of SGCs.© 2015 American Academy of Pain Medicine. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.

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