Linarin attenuates oxaliplatin-induced neuropathic pain by inhibiting NF-κB/NLRP3 signaling pathway
Résumé
Purpose: To assess the therapeutic effects of linarin on chemotherapy-induced peripheral neuropathy (CINP) in rats.Methods: A CINP rat model was established using oxaliplatin. The rats were divided into control, CINP, and two linarin treatment groups (20 mg/kg/day and 40 mg/kg/day). Observations were made at various time points, assessing weight gain, mechanical withdrawal thresholds, cold allodynia response, and thermal pain sensitivity. Additionally, the expression levels of various inflammatory factors (IL-1β, IL-6, IL-10, and IL-17), proteins related to glial and neuronal activation (IBA-1, GFAP, c-fos), and proteins linked to NF-κB/NLRP3 signaling (ASC, caspase-1, p65, and p-p65) were evaluated in rat spinal cord tissue.Results: Linarin treatment resulted in improved weight gain, mechanical threshold, decreased withdrawal response, and enhanced paw withdrawal latency (p < 0.001) compared to the CINP group. These improvements or mitigations were more pronounced in the 40 mg/kg/day linarin group. Linarin inhibited the expression of inflammatory factors IL-1β, IL-6, and IL-17 (p < 0.001) but enhanced IL-10 expression (p < 0.001). The activation of microglia, astrocytes, and neurons, as indicated by IBA-1, GFAP, and c-fos (p < 0.001) proteins, was significantly reduced with linarin, especially at the higher dose. Linarin also suppressed the expression of ASC, caspase-1, p65, and p-p65 (p < 0.001) proteins, associated with the NF-κB/NLRP3 signaling pathway.Conclusion: Our study indicates that linarin may serve as a potential therapeutic agent for managing CINP. The beneficial effects of linarin are likely mediated through its immunomodulatory effects and the inhibition of the NF-κB/NLRP3 signaling pathway. Further research is needed to confirm these findings in clinical settings.
Citer ce document
Accès au document
Texte intégral en lecture en ligne, réservé aux abonnés SPHAERO et aux membres de l'institution. Se connecter
Voir l'article sur le site de la revueAuteur(s)
Statistiques
Consultations : 1
Téléchargements : 0