Paeoniflorin attenuates chronic constriction injury-induced neuropathic pain by suppressing spinal NLRP3 inflammasome ac
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Inflammopharmacology
ORIGINAL ARTICLE
Paeoniflorin attenuates chronic constriction injury‑induced neuropathic pain by suppressing spinal NLRP3 inflammasome activation Pei Liu1 · Jianjun Cheng1 · Shuai Ma1 · Jianyu Zhou1 Received: 21 April 2020 / Accepted: 20 June 2020 © Springer Nature Switzerland AG 2020
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. Keywords NLRP3 · Inflammasome · Caspase-1 · Neuropathic pain · Nrf2 · Paeoniflorin
Introduction Neuropathic pain is one of the most ubiquitous diseases worldwide. Owing to a lack of knowledge on the mechanisms underlying pathological pain, the treatment of neuropathic pain via conventional methods is difficult (Peng et al. 2017; Ji et al. 2019; Meyer et al. 2019; Cornelius et al. 2013). Therefore, it is necessary to clarify the mechanisms underlying neuropathic pain to identify more effective pharmacological treatments. Accumulating evidence supports the vital role of neuroinflammation in the pathogenesis of neuropathic pain, which is now considered a neuroimmune disorder (Myers et al. 2006; Chen et al. 2018; Yadav Pei Liu and Jianjun Cheng have contributed equally to this work and share first authorship. * Jianyu Zhou [email protected] 1
Hebei Key Laboratory of Research and Development for Chinese Medicine, Chengde Medical University, Chengde 067000, Hebei, P. R. China
and Surolia 2019). Previous studies have demonstrated that increased interleukin (IL)-1β expression is observed in damaged nerves, the dorsal root ganglia, neurons, and glial cells in the spinal cord and pain-related brain regions in animals and patients with underlying neuropathic pain (de Rivero Vaccari et al. 2009; Wei et al. 2009; Murasawa et al. 2019; Pollema-Mays et al. 2014; Morioka et al. 2015; Jiang et al. 2016). Moreover, IL-1β is sho
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