Enhanced RAGE Expression in the Dorsal Root Ganglion May Contribute to Neuropathic Pain Induced by Spinal Nerve Ligation in Rats

Pain Medicine : the Official Journal of the American Academy of Pain Medicine
Xiangnan LiHongbin Yuan

Abstract

There 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. Experimental study before and after spinal nerve ligation (SNL) surgery. Caged in a controlled environment. Male Sprague-Dawley rats. A 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. After 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. RAGE signaling may contribute to the pain hypersensitivity ...Continue Reading

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Citations

Jun 12, 2019·Pain Research & Management : the Journal of the Canadian Pain Society = Journal De La Société Canadienne Pour Le Traitement De La Douleur·Xueru XuRongguo Liu
Aug 28, 2021·Biomedicines·Kjeld Morten MohrChristian Bjerggaard Vaegter

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