Fucoidan alleviated dextran sulfate sodium-induced ulcerative colitis with improved intestinal barrier, reshaped gut microbiota composition and promoted autophagy in male C57BL/6 mice

While previous research has unveiled the remedial effects of fucoidan, an extract from marine algae, on Ulcerative Colitis (UC), the precise mechanisms remain elusive. Animal studies have suggested a connection between autophagy and the beneficial influences of fucoidan intervention. We thus hypothesized that fucoidan's alleviative effects on DSS-induced UC could be ascribed to autophagy. For our study, we chose thirty-six male C57BL/6 mice and administered 100 or 400 mg/(kg·bw·day) of fucoidan via gavage for five consecutive weeks. During the last week, the mice were given 3% dextran sulfate sodium (DSS) in drinking water to induce UC. In contrast to the DSS-induced UC model, fucoidan intervention prevented DSS-induced body weight loss, mitigated colon shortening, improved colon mucosa damage, enhanced the intestinal barrier, and reduced serum inflammatory factor concentrations. Furthermore, fucoidan intervention reshaped the gut microbiota compositions, increased the relative abundance of Bacteroidota, Muribaculaceae_unclassified, Clostridiales_unclassified and Lachnospiraceae_NK4A136_group , and decreased the relative abundance of Firmicutes, Proteobacteria and Escherichia-Shigella , which led to a lower Firmicutes/Bacteroidota ratio. Additionally, fucoidan treatment enhanced autophagy, as evidenced by upregulated protein expressions of BECLIN1, ATG5, ATG7, and an increased LC3-II/LC3-I ratio. Our findings corroborated the ameliorating effects of fucoidan intervention on DSS-induced UC through autophagy activation, reorganization of gut microbiota, and fortification of the intestinal barrier. This lends support to the therapeutic potential of fucoidan as a natural bioactive ingredient for future UC treatments in humans.

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