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Scleroglucan ameliorates dextran sulfate sodium-induced ulcerative colitis and gut microbiota dysbiosis in mice.

Created on 26 Jul 2026

Authors

Yiyi Zhao, Yanlong Wen, Dafang Yin, Fuqin Yang, Yadong Zhong, Jielun Hu

Published in

International journal of biological macromolecules. Pages 153708. Jul 25, 2026. Epub Jul 25, 2026.

Abstract

β-1,3/1,6-Glucans exhibit significant potential as therapeutic agents for ulcerative colitis (UC); nevertheless, most existing studies have focused on yeast β-glucans. In the current research, we assessed the therapeutic effects of scleroglucan (SCL), a β-1,3/1,6-glucan produced from the fungus Sclerotium rolfsii, by using a dextran sulfate sodium (DSS)-induced mouse model. SCL treatment significantly attenuated DSS-induced body weight loss from 18.45% to 14.69%, reduced the disease activity index from 3.83 to 3.11, decreased colonic TNF-α and MPO levels, and restored IL-10 concentrations (p < 0.05). SCL also promoted goblet cell proliferation and upregulated Muc2 gene expression (p < 0.05), but had no significant effects on colon length and tight junction proteins. Additionally, SCL significantly increased cecal acetate to 10.82 μmol/g, propionate to 3.87 μmol/g, butyrate to 7.13 μmol/g, and valerate to 1.16 μmol/g, compared with the respective levels of 3.11, 1.61, 1.67, and 0.60 μmol/g in the DSS group. Consistently, enhanced colonic mRNA expression of GPR41, GPR43, and GPR109A was seen with the SCL group than the DSS group (p < 0.05). SCL also remodeled gut microbiota composition, and significantly elevated Bacteroidetes, Lactobacillus and Ruminococcus, and reduced Firmicutes (p < 0.05), a microbial profile associated with attenuated colitis severity. Taken together, these findings indicate that SCL effectively mitigated DSS-induced colitis, emphasizing its potential as a bioactive polysaccharide for developing functional foods to assist UC nutritional intervention.

PMID:
42501847
Bibliographic data and abstract were imported from PubMed on 26 Jul 2026.

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