Abstract
Neuropathic pain remains one of the most common pain conditions worldwide. Accumulating evidence shows that activation of the NOD-like receptor protein 3 (NLRP3) inflammasome contributes to the pathogenesis of neuropathic pain, although the role of the NLRP3 inflammasome in neuropathic pain has not yet been fully elucidated. In animal models of neuropathic pain, paeoniflorin (PF) was shown to have analgesic, anti-inflammatory, and antidepressant effects. However, the role of the NLRP3 inflammasome in the analgesic properties of PF has not yet been studied. In this study, we aimed to confirm whether activation of the NLRP3 inflammasome in the spinal cord was involved in the development of neuropathic pain and whether PF could be an effective treatment for this type of pain. We found that activation of the NLRP3 inflammasome mediated the development of neuropathic pain following chronic constriction injury of the sciatic nerve and that PF attenuated neuropathic pain by inhibiting NLRP3 inflammasome activation. Moreover, PF enhanced the translocation of the transcription factor nuclear factor erythroid 2-related factor 2 into the nucleus and suppressed nuclear factor-kappa B activity in the spinal cord. These results suggest that PF may be a potential therapeutic agent for neuropathic pain.