Pain research & management · 2026
The Specialized Proresolving Mediator Maresin 1 Alleviated Neuropathic Pain Exacerbated by High-Fat Diet via Regulating Neuroinflammation.
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Zhang Li, Hu Ran, Qin Kexin, Wang Xue, Wu Chen, Liu Zichen, Shao Xiangqi, Sun Jianru, Liu Yang, Xiao Saisong, Ren Huilong, Liu Fan, Liu Guokai
Аннотация
BACKGROUND: Clinical observations have suggested an association between a high-fat diet (HFD) and neuropathic pain (NP). Studies also revealed that maresin 1 (MaR1) can regulate macrophage phagocytosis, modulate tissue repair and inflammatory resolution, and influence the progression of NP. However, the specific regulatory mechanisms of MaR1 in HFD-induced NP remain unclear.
OBJECTIVE: The aim of this study is to explore the effect of MaR1 on neuroinflammation in mice with NP induced by an HFD.
METHODS: A tibial nerve crush model with a HFD was used to establish HFD-induced chronic pain. The paw withdrawal threshold (PWT), which reflects mechanical allodynia, was measured to evaluate changes in pain-related behavior. Immunofluorescence was used to detect the relative number of macrophages and microglia, and the expression of growth-associated protein 43 (GAP43), while qPCR was used to measure the levels of proinflammatory cytokines.
RESULTS: HFD consumption exacerbates nerve injury-induced NP formation and upregulates GAP43 expression. Macrophage infiltration and proinflammatory cytokine expression were increased in the DRGs of HFD-induced nerve injury mice. Intrathecal injection of the specialized proresolving mediator MaR1 alleviated nerve injury-induced chronic pain and decreased GAP43 expression in HFD-fed mice. Furthermore, MaR1 decreased proinflammatory macrophage migration in the damaged tibial nerves and DRGs of HFD-induced nerve injury model mice.
CONCLUSIONS: The specialized proresolving mediator MaR1 can reduce neuroinflammation and GAP43 expression in the DRG and injured nerve fibers and alleviate NP in HFD-fed mice.
OBJECTIVE: The aim of this study is to explore the effect of MaR1 on neuroinflammation in mice with NP induced by an HFD.
METHODS: A tibial nerve crush model with a HFD was used to establish HFD-induced chronic pain. The paw withdrawal threshold (PWT), which reflects mechanical allodynia, was measured to evaluate changes in pain-related behavior. Immunofluorescence was used to detect the relative number of macrophages and microglia, and the expression of growth-associated protein 43 (GAP43), while qPCR was used to measure the levels of proinflammatory cytokines.
RESULTS: HFD consumption exacerbates nerve injury-induced NP formation and upregulates GAP43 expression. Macrophage infiltration and proinflammatory cytokine expression were increased in the DRGs of HFD-induced nerve injury mice. Intrathecal injection of the specialized proresolving mediator MaR1 alleviated nerve injury-induced chronic pain and decreased GAP43 expression in HFD-fed mice. Furthermore, MaR1 decreased proinflammatory macrophage migration in the damaged tibial nerves and DRGs of HFD-induced nerve injury model mice.
CONCLUSIONS: The specialized proresolving mediator MaR1 can reduce neuroinflammation and GAP43 expression in the DRG and injured nerve fibers and alleviate NP in HFD-fed mice.