ArticleJournal of advanced research2026
Hyodeoxycholic acid relieves neuropathic pain by activating farnesoid X receptor signaling.
Article in Journal of advanced research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Expansion resistance against genotoxicFrontiers in microbiology · 2026Article
- The role of gut microbiota in neuropathic pain: insights into immune mechanisms.The journal of headache and pain · 2025Review
- Gut-Spinal Cord Axis in Spinal Cord Injury: Bidirectional Inflammatory Mechanisms and Microbiota-Targeted Therapeutic Strategies.Journal of inflammation research · 2025Review
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNeuropathic pain, is a chronic condition stemming from nervous system injuries. The farnesoid X receptor (FXR), primarily expressed in the liver and intestines, plays a crucial role in regulating bile acids and lipids metabolism. Emerging evidence suggests that bile acids might influence neural function through FXR modulation.
objectiveTo investigate the specific role of intestinal FXR in the modulation of neuropathic pain.
methodsA neuropathic pain model was established in mice through ligation of the lumbar 4 spinal nerve (SNL). FXR expression was detected in the distal ileum and spinal cord. The baseline pain threshold and pain-related behaviors were evaluated in FXR gene knockout (Fxr
resultsNeuropathic pain was associated with reduced FXR levels in the gut and spinal cord, accompanied by decreased bile acid levels, especially HDCA. FXR deficiency lowered the pain threshold, whereas treatment with INT-747 or HDCA relieved pain in SNL mice. Activation of FXR restored intestinal barrier integrity, balanced microbiota, reduced inflammation, and decreased microglial activation. HDCA alleviated pain by modulating FXR activity, increasing peroxisome proliferator-activated receptor gamma (PPAR-γ) expression and reducing abnormal matrix metalloproteinase-2 (MMP-2) and matrix metalloproteinase-2 (MMP-9) activation.
conclusionThis research highlights a critical link between FXR levels and neuropathic pain. Manipulating FXR activity with INT-747 or HDCA not only reduced pain severity but also strengthened intestinal barriers and dampened inflammatory responses, suggesting the potential of FXR-targeted therapies in effectively managing neuropathic pain.
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