ArticleMolecular pain
Evodiamine attenuates chemotherapy-induced peripheral neuropathy by mediating macrophage M2 polarization and inhibiting the upregulation of the p38 MAPK-TRPV1 axis in rat dorsal root ganglia.
Article in Molecular pain. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- T cell-dependent modulation of pain behaviors in a rat model of recurring paclitaxel-induced peripheral neuropathy.Brain, behavior, & immunity - health · 2026Article
- Ex vivo modulation of monocyte/macrophage phenotypes by all-trans retinoic acid in chemotherapy-induced peripheral neuropathy.Molecular biology reports · 2026Article
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7 authors.
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Abstract
purposeTo investigate evodiamine's analgesic effects and molecular mechanisms on chemotherapy-induced peripheral neuropathy (CIPN), focusing on the p38/MAPK-TRPV1 signaling axis and macrophage polarization in dorsal root ganglia (DRG).
methodsA paclitaxel-induced CIPN rat model was established with behavioral assessments via von Frey and thermal hyperalgesia tests. TRPV1, TRPV4, and inflammatory cytokine expression were analyzed using qRT-PCR, ELISA, and Western blot. Macrophage infiltration and polarization were evaluated by flow cytometry and immunofluorescence. Mechanistic studies utilized macrophage-conditioned media from RAW264.7 cells and clodronate liposome-mediated macrophage depletion to establish causal relationships between macrophage polarization and nociceptive behavior.
resultsEvodiamine dose-dependently alleviated paclitaxel-induced mechanical and thermal allodynia both acutely and preventively. It selectively inhibited upregulation of TRPV1 without affecting TRPV4 and reduced pro-inflammatory cytokine levels (TNF-α, IL-1β, IL-6, MCP-1) in the DRG. Evodiamine significantly reduced F4/80+ macrophage infiltration and shifted macrophage polarization from a pro-inflammatory M1 phenotype (decreased MCP1, CD86) to an anti-inflammatory M2 phenotype (increased CD163, CD206). Notably, macrophage-conditioned medium experiments revealed that evodiamine indirectly modulates neuronal TRPV1 expression through macrophage-derived factors. Furthermore, evodiamine attenuated paclitaxel-induced p38 MAPK phosphorylation in DRG neurons, with selective p38 MAPK inhibition by SB203580 confirming this pathway's critical involvement in TRPV1 regulation and pain modulation.
conclusionEvodiamine alleviates CIPN through a novel neuroimmune mechanism involving M2 macrophage polarization and inhibition of the p38/MAPK-TRPV1 axis in DRG neurons. These findings establish macrophage polarization as a key therapeutic target and highlight evodiamine's potential as a natural therapeutic agent for CIPN management.
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