ArticleCell communication and signaling : CCS2025
Resveratrol alleviates IBD-associated neuropsychiatric comorbidities via microbiota-dependent arginine metabolism reprogramming and microglial M2 polarization through gut-brain axis.
Article in Cell communication and signaling : CCS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Gut Microbiota-Dependent Tryptophan Metabolism Drives the Therapeutic Effects of Baitouweng Tang in Colitis via the AhR Pathway.Food science & nutrition · 2026Article
- Adhesion-Enhanced Engineered Probiotic for Prolonged Intestinal Retention and Calprotectin-Responsive IBD Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Oral Sodium Hyaluronate Reshapes Gut Microbiota Composition and Suppresses the LPS-TLR4/NF-κB Pathway to Exert Neuroprotection in MPTP-Induced Parkinson's Disease.International journal of molecular sciences · 2026Article
- Neuroglobin: A New Player in the Gut-Brain Axis.International journal of molecular sciences · 2026Review
- Review
- Age-Dependent Alterations in Intestinal Barrier Function: Involvement of Microbiota and TLR4 Signaling.Biology · 2026Article
- Resveratrol and the NLRP3 Inflammasome: Unlocking the Anti-inflammatory Potential of a Natural Compound.Current pharmaceutical design · 2026Review
- Gut microbiota and inflammatory bowel disease: mechanisms, clinical implications, and future directions.Molecular biology reports · 2025Review
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Authors and funding
19 authors.
Funding
Abstract
Inflammatory bowel disease (IBD) is intricately linked to neuropsychiatric comorbidities through gut-brain axis dysregulation. This study demonstrates that resveratrol (RSV), a natural polyphenol, alleviates DSS-induced colitis-associated anxiety and depression by reprogramming the microbiota─metabolite-barrier network. RSV (100 mg/kg/day) ameliorated DSS-associated anxiety-like behaviors in open field tests (peripheral zone time ↓12.6%, P< 0.0001) and depression-like phenotypes (TST immobility ↓31.0%, P = 0.0004). It restored colonic barrier integrity via ZO-1 mRNA upregulation (↑80.4%, P < 0.0001) and PAS score recovery (↑29.6%, P < 0.0001), while reducing systemic inflammation (serum LPS ↓31.9%, TNF-α ↓29.9%; P < 0.0001) vs. DSS. Crucially, RSV attenuated neuroinflammation by enhancing brain ZO-1 protein expression (↑146.1%, P = 0.0016), suppressing TLR4/MyD88/NF-κB signaling (TLR4 mRNA ↓68.8%, MyD88 protein ↓48.8%; P < 0.05), and promoting M2 microglial polarization (CD206 protein ↑171.9%, P = 0.0003) vs. DSS. Multi-omics integration revealed RSV’s dual regulatory mechanism: ① Suppression of the pro-inflammatory Turicibacter4-guanidinobutanoic acid axis (↓42% and ↓37%, respectively; P < 0.01), disrupting LPS─TLR4─MyD88 cascades; ② Enrichment of barrier-protective Muribaculum (↑419%) and Dubosiella (↑208%), driving polyamine synthesis (spermidine ↑92%, spermine ↑38%) vs. DSS to reinforce gut-brain barriers. Spearman correlations confirmed Turicibacter-4-guanidinobutanoic acid-LPS-MyD88 interactions(r = 0.658-0.865) and Dubosiella-spermine-ZO-1 associations (r = 0.539-0.725). Conclusions: These findings establish RSV as a microbiota-metabolite modulator that redirects arginine metabolism from a pro-inflammatory bypass to polyamine-mediated barrier repair, offering novel therapeutic strategies for IBD-related neuropsychiatric complications. The integrated "microbe-metabolite-neuroimmune" axis provides mechanistic insights into gut-brain crosstalk, emphasizing dual-barrier restoration as a critical intervention node.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.