What question did this study set out to answer?

The study aims to evaluate the protective effects of cooked oat bran on DSS-induced colitis in mice.

March 10, 2026Open Access

Oat bran ameliorated DSS-induced mice colitis by suppressing inflammation and enriching beneficial metabolites derived from gut microbiota

Key Points

The study aims to evaluate the protective effects of cooked oat bran on DSS-induced colitis in mice.
Mice were administered dextran sulfate sodium to induce colitis.
Cooked oat bran was supplemented to assess its effects on symptoms and microbiota.
Histological analyses and metabolic profiling were conducted.
Cytokine levels were measured to evaluate immune response.
Correlation analyses were used to assess relationships between microbiota and metabolites.
COB reduced body weight loss and colonic shortening in mice with colitis.
COB restored intestinal barrier function by upregulating Claudin-1 expression.
Pro-inflammatory cytokines were significantly suppressed, while IL-10 levels increased.
COB enriched beneficial gut microbiota, particularly Akkermansia and Bifidobacterium.
Metabolomics revealed upregulation of sphingolipid metabolites associated with gut health.

Abstract

Inflammatory bowel disease (IBD) is characterized by chronic gastrointestinal inflammation and gut microbiota dysbiosis. This study evaluated the protective effects of cooked oat bran (COB) on dextran sulfate sodium (DSS)-induced colitis in mice. COB supplementation significantly attenuated clinical symptoms, including body weight loss, colonic shortening, and histological damage. Mechanistically, COB restored intestinal barrier function by upregulating Claudin-1 expression and rebalanced immune responses by suppressing pro-inflammatory cytokines (TNF-α, IFN-γ, and IL-1β) while enhancing anti-inflammatory IL-10 levels. Furthermore, COB modulated the gut microbiota by enriching beneficial taxa, notably Akkermansia and Bifidobacterium , and promoting the production of short-chain fatty acids (SCFAs), including acetate, propionate, and butyrate. Untargeted metabolomics revealed that COB significantly altered metabolic pathways, characterized by the upregulation of sphingolipid metabolism-related metabolites, specifically sphinganine and sphingosine-1-phosphate (S1P). Correlation analysis highlighted a positive association between Akkermansia abundance and sphinganine levels, suggesting a functional microbiota-metabolite axis. Collectively, these findings indicate that COB is a promising functional dietary strategy for mitigating IBD via the synergistic regulation of inflammation, barrier integrity, and the gut microbiome. • DSS-induced colitis is alleviated and intestinal barrier integrity restored by COB. • COB reshapes gut microbiota, enriching Akkermansia and Bifidobacterium and enhancing SCFA production. • Fecal sphingolipid metabolism is improved by COB, elevating sphinganine/S1P and suppressing TNF-α. • COB provides a potential dietary intervention strategy for IBD.

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