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Background <p>Neuropathic pain is characterized by hyperalgesia, allodynia, and inflammation and it is often resistant to treatment. The formyl peptide receptor 2 (ALX/FPR2), a G-protein-coupled receptor, has been implicated in resolving inflammation, making its agonist, Resolvin D1 (RvD1), a potential therapeutic agent. Previous studies suggest that RvD1 alleviates neuropathic pain via anti-inflammatory effects, but its mechanisms remain unclear, particularly in relation to microglial activation and the brain-derived neurotrophic factor (BDNF)/TrkB signaling pathway.</p> Objective <p>To investigate the analgesic effects of RvD1 in a spared nerve injury (SNI) model of neuropathic pain and explore its mechanisms through the regulation of neuroinflammation and the BDNF/TrkB signaling pathway.</p> Methods <p>SNI mice received intrathecal RvD1 at varying doses (10–40&#xa0;ng) to determine its efficacy in reducing mechanical allodynia and thermal sensitivity. The anti-inflammatory effects of RvD1 were assessed using ELISA, immunofluorescence, and western blotting to measure the expression of pro-inflammatory cytokines and BDNF. The involvement of ALX/FPR2 and TrkB receptors was further examined using antagonists Boc2 and K252a.</p> Results <p>RvD1 significantly reduced mechanical and thermal allodynia in SNI mice in a dose-dependent manner. RvD1 also decreased microglial activation and expression of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6) and BDNF in both in vivo and in vitro models. These effects were reversed by Boc2 and K252a, confirming that the analgesic actions of RvD1 are mediated via the ALX/FPR2 receptor and inhibition of BDNF/TrkB signaling.</p> Conclusion <p>RvD1 alleviates neuropathic pain by reducing neuroinflammation through the ALX/FPR2 receptor and suppressing BDNF/TrkB signaling. These findings suggest RvD1 as a promising therapeutic agent for neuropathic pain management.</p>

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Resolvin D1 accelerates resolution of neuroinflammation by inhibiting microglia activation through the BDNF/TrkB signaling pathway

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年3月20日

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  • Cunju Bo,
  • Xiaoming Liu,
  • Yongjian Liu,
  • Lingjun Xu,
  • Qiaodong Huang

摘要

Background

Neuropathic pain is characterized by hyperalgesia, allodynia, and inflammation and it is often resistant to treatment. The formyl peptide receptor 2 (ALX/FPR2), a G-protein-coupled receptor, has been implicated in resolving inflammation, making its agonist, Resolvin D1 (RvD1), a potential therapeutic agent. Previous studies suggest that RvD1 alleviates neuropathic pain via anti-inflammatory effects, but its mechanisms remain unclear, particularly in relation to microglial activation and the brain-derived neurotrophic factor (BDNF)/TrkB signaling pathway.

Objective

To investigate the analgesic effects of RvD1 in a spared nerve injury (SNI) model of neuropathic pain and explore its mechanisms through the regulation of neuroinflammation and the BDNF/TrkB signaling pathway.

Methods

SNI mice received intrathecal RvD1 at varying doses (10–40 ng) to determine its efficacy in reducing mechanical allodynia and thermal sensitivity. The anti-inflammatory effects of RvD1 were assessed using ELISA, immunofluorescence, and western blotting to measure the expression of pro-inflammatory cytokines and BDNF. The involvement of ALX/FPR2 and TrkB receptors was further examined using antagonists Boc2 and K252a.

Results

RvD1 significantly reduced mechanical and thermal allodynia in SNI mice in a dose-dependent manner. RvD1 also decreased microglial activation and expression of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6) and BDNF in both in vivo and in vitro models. These effects were reversed by Boc2 and K252a, confirming that the analgesic actions of RvD1 are mediated via the ALX/FPR2 receptor and inhibition of BDNF/TrkB signaling.

Conclusion

RvD1 alleviates neuropathic pain by reducing neuroinflammation through the ALX/FPR2 receptor and suppressing BDNF/TrkB signaling. These findings suggest RvD1 as a promising therapeutic agent for neuropathic pain management.