Attenuation of DSS induced colitis by Dictyophora indusiata polysaccharide (DIP) via modulation of gut microbiota and inflammatory related signaling pathways
[Display omitted] •DIP oral administration alleviates DSS induced colitis symptoms in mice model.•DIP attenuates intestinal barrier integrity and improved histological architecture.•DIP regulates oxidative stress and inflammatory cytokines secretion.•DIP modulates inflammatory signaling pathways and...
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Veröffentlicht in: | Journal of functional foods 2020-01, Vol.64, p.103641, Article 103641 |
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Format: | Artikel |
Sprache: | eng |
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•DIP oral administration alleviates DSS induced colitis symptoms in mice model.•DIP attenuates intestinal barrier integrity and improved histological architecture.•DIP regulates oxidative stress and inflammatory cytokines secretion.•DIP modulates inflammatory signaling pathways and gut microbiome composition.
Inflammatory bowel disease (IBD) is a lifelong chronic inflammation of the gastrointestinal tract. Polysaccharides from mushrooms have been extensively used to treat inflammatory diseases including IBD. Dictyophora indusiata polysaccharide (DIP) modulates gut microbiota and alleviate inflammatory reactions; however, its effect on ulcerative colitis (UC) is yet to explore. In this study DIP effect on DSS induced colitis was determined. Our findings revealed that DIP treatment alleviated the severity of colitis, especially at the high dose. The histopathological alterations and gut epithelial integrity were ameliorated. The inflammatory reactions and oxidative stress were improved. Moreover, proinflammatory cytokines were reduced, conversely, anti-inflammatory cytokines and tight junction proteins (TJs) were elevated. Furthermore, Illumina MiSequencing exhibited perturbation of bacterial community upon DSS treatment; however, the bacterial shift was reversed after DIP treatment. Inclusively, our findings suggest mushroom polysaccharides may have a potential therapeutic effect against colitis and inflammatory-related diseases. |
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ISSN: | 1756-4646 2214-9414 |
DOI: | 10.1016/j.jff.2019.103641 |