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.

神经性疼痛仍然是世界范围内最常见的疼痛状况之一。越来越多的证据表明，尽管尚未完全阐明NLRP3炎性小体在神经性疼痛中的作用，但NOD样受体蛋白3（NLRP3）炎性小体的激活有助于神经性疼痛的发病机理。在神经性疼痛的动物模型中，pa药苷（PF）具有镇痛，抗炎和抗抑郁作用。但是，尚未研究NLRP3炎性小体在PF的止痛特性中的作用。在这项研究中，我们旨在确认脊髓中NLRP3炎性小体的激活是否与神经性疼痛的发展有关，以及PF是否可以有效治疗此类疼痛。我们发现，NLRP3炎性小体的激活介导了坐骨神经慢性压迫性损伤后神经性疼痛的发展，PF通过抑制NLRP3炎性小体的激活来减轻神经性疼痛。此外，PF增强了转录因子核因子红系2相关因子2向核内的转运，并抑制了脊髓中核因子-κB的活性。这些结果表明，PF可能是神经性疼痛的潜在治疗剂。PF增强了转录因子核因子红系2相关因子2向核内的转运，并抑制了脊髓中核因子-κB的活性。这些结果表明，PF可能是神经性疼痛的潜在治疗剂。PF增强了转录因子核因子红系2相关因子2向核内的转运，并抑制了脊髓中核因子-κB的活性。这些结果表明，PF可能是神经性疼痛的潜在治疗剂。