REVIEW article
Front. Cell. Infect. Microbiol.
Sec. Bacteria and Host
Volume 15 - 2025 | doi: 10.3389/fcimb.2025.1626614
This article is part of the Research TopicEffects of Dietary Nutrients on Intestinal Microbiome: Insights into Gastrointestinal Diseases in Animals Volume IIView all articles
Fucoidan as a Therapeutic Agent for Ulcerative Colitis: Mechanisms of Action and Modulation of the Gut Microbiota
Provisionally accepted
- Hunan Agricultural University, Changsha, China
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Ulcerative colitis (UC), a chronic inflammatory bowel disease driven by gut dysbiosis, immune dysregulation, and oxidative stress, lacks universally effective therapies. Fucoidan (FCD), a sulfated polysaccharide derived from brown algae, has emerged as a multifaceted therapeutic candidate due to its anti-inflammatory, antioxidant, and immunomodulatory properties. This review synthesizes FCD's mechanisms in UC pathogenesis, emphasizing its suppression of NF-κB and MAPK signaling pathways to reduce proinflammatory cytokines (e.g., IL-6, TNF-α) and regulate TLR-mediated macrophage polarization. FCD enhances intestinal barrier integrity via upregulation of tight junction proteins (Claudin-1, ZO-1) and mucin MUC2 expression, while remodeling gut microbial ecology through enrichment of SCFAs-producing bacteria (e.g., Ruminococcaceae) and suppression of pathogens (Escherichia coli, Candida albicans). Preclinical studies highlight LMWF as a superior candidate, demonstrating enhanced bioavailability and efficacy in mitigating DSS-induced colitis. Despite its promise, challenges persist in structural heterogeneity (source-and extractiondependent), scalable production of LMWF, and insufficient pharmacokinetic data.Emerging strategies-including nanoparticle-based delivery systems and structural modifications (cross-linking, covalent bonding)-aim to overcome bioavailability limitations. This review underscores FCD's potential as a functional food or adjuvant therapy for UC, while advocating for rigorous clinical validation to bridge translational gaps, Enrichment of SCFAs-producing taxa and suppression of pathobionts (Escherichia coli, Candida albicans), mediated through prebiotic fermentation.Suppression of NF-κB activation via IκBα stabilization and inhibition of p65 nuclear translocation, and downregulation of MAPK phosphorylation (ERK1/2, JNK, p38), reducing proinflammatory cytokines (IL-6, TNF-α, IL-1β). FCD can be used as a potential treatment for UC.
Keywords: fucoidan, ulcerative colitis, Gut Microbiota, Toll-like receptors (TLRs), Oxidative Stress, Inflammation
Received: 11 May 2025; Accepted: 13 Jun 2025.
Copyright: © 2025 Zhang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Yating Zhang, Hunan Agricultural University, Changsha, China
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