Inflammatory bowel disease (IBD) is characterized by persistent intestinal inflammation and gut microbiota dysbiosis. The study investigated the protective effects of Ganoderma lucidum polysaccharide (GLP) and ganoderic acid A (GAA) administered individually and in combination on dextran sulfate sodium (DSS)-induced colitis in mice. Disease activity index (DAI), colon length, histopathology, serum inflammatory cytokines (TNF-α, IL-1β, IL-6), TLR4/NF-κB pathway proteins, gut microbiota composition, and short-chain fatty acids (SCFAs) were evaluated. Combination therapy of GLP and GAA (GL-PA) significantly ameliorated body weight loss, reduced DAI scores, and restored colon length compared to individual treatments (P < 0.05). Histopathological analysis revealed preserved crypt architecture and reduced inflammatory infiltration. GL-PA markedly suppressed serum cytokine levels and inhibited TLR4/NF-κB activation more effectively than GLP or GAA alone (P < 0.05). Microbiota analysis showed GL-PA restored gut diversity, increased Firmicutes/Bacteroidetes ratio, promoted beneficial bacteria (Lactobacillus, Turicibacter) while suppressing pathogenic bacteria (Bacteroides, Escherichia-Shigella, and Desulfovibrionaceae). GL-PA significantly enhanced SCFAs production, particularly propionate and butyrate (P < 0.01). Correlation analysis revealed associations between harmful bacteria and inflammatory markers, while beneficial bacteria correlated with SCFAs levels. The combination exhibits synergistic protective effects through dual mechanisms: inflammatory pathway suppression and gut microbiota homeostasis restoration. GL-PA represents a promising natural therapeutic strategy for IBD treatment.
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Open Access
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To further explore and develop tartary buckwheat (Fagopyrum tataricum), a specialty agricultural product of Liangshan, Sichuan Province, this study investigated the effect and mechanism of action of tartary buckwheat seedling powder (TBSP) on dextran sulfate sodium (DSS)-induced ulcerative colitis (UC) and the gut microbiota in mice.
A mouse model of UC was established using 3% DSS. The mice received TBSP via gavage at doses of 100 or 400 mg/kg. Changes in body mass, disease activity index (DAI) score, organ indices, colon length, histopathological damage, colonic inflammatory cytokine levels, protein expression of nuclear factor kappa B (NF-κB) and inhibitor of nuclear factor kappa B alpha (IκBα), alterations in the gut microbiota, and short-chain fatty acid (SCFA) contents were evaluated.
TBSP significantly ameliorated pathological states in UC mice, including body mass loss, increased DAI score, colon shortening, intestinal barrier damage, elevated inflammatory cytokine levels, and overactivation of the NF-κB signaling pathway, in a dose-response manner. TBSP modulated the structure of the gut microbiota in UC mice. At the phylum level, it decreased the relative abundances of Proteobacteria and Desulfobacterota while increasing that of Verrucomicrobiota. At the genus level, it increased the relative abundances of barrier repair-associated genera such as Akkermansia and Lactobacillus.
TBSP alleviated colitis symptoms by regulating the gut microbiota, reducing inflammatory cytokine levels, and repairing the colonic mucosal barrier in UC mice. Therefore, TBSP is a promising functional food resource.
Open Access
Issue
To promote the high-value utilization and industrial development of tartary buckwheat and to develop functional products based on tartary buckwheat bran (TBB), this study analyzed the basic composition and investigated the ameliorative effect of TBB on dextran sodium sulfate (DSS)-induced ulcerative colitis (UC) in mice and its anti-inflammatory mechanism.
The contents of protein, fat, total dietary fiber, ash, and starch in TBB were determined. The ameliorative effect on UC induced by 3% DSS in mice was evaluated by hematoxylin and eosin staining of colon sections, enzyme-linked immunosorbent assay (ELISA), Western blotting, gas chromatography (GC), and 16S rDNA high-throughput sequencing.
Compared with the model group, TBB significantly alleviated body mass loss, reduced appetite, shortened colon length, and rectal bleeding in mice suffering from UC, mitigated colon crypt damage and goblet cell reduction, suppressed the secretion of pro-inflammatory cytokines, and reduced inflammation through inhibiting nuclear factor kappa-B (NF-κB) signaling pathway. It also restored the levels of acetic acid, propionic acid, butyric acid, isobutyric acid, valeric acid, and total short-chain fatty acids in the intestine while modulating the gut microbiota composition, especially enhancing the relative abundance of g__Akkermansia and g__Lactobacillus.
TBB contains a high level of dietary fiber, which can significantly alleviate UC. This finding provides a scientific basis for the high-value utilization of TBB as a functional food ingredient.
Open Access
Research Article
Issue
Dendrobium officinale oligosaccharides (DOO), as a novel prebiotic, offer promising therapeutic potential for the treatment of inflammatory diseases. In this study, the alleviating effect of DOO on dextran sulfate sodium (DSS)-induced chronic colitis in mice was investigated. DOO treatment relieved the main symptoms of weight loss, colon shortening, and bloody stool caused by colitis. DOO ameliorated histopathological colon tissue damage and reduced levels of pro-inflammatory factors (TNF-α, IL-6, IL-1β). Western blot results suggested that DOO downregulated the phosphorylation levels of key proteins in the NF-κB signaling pathway, including IKKα/β, IκBα and p65. 16S rRNA sequencing suggested that DOO altered the diversity and composition of gut microbiota in DSS-induced mice. It promoted the intestinal colonization of beneficial bacteria such as Dubosiella, Lactobacillus and Alistipes, and inhibited the abnormal overgrowth of Akkermansia. Furthermore, DOO increased the secretion of short-chain fatty acids (SCFAs) such as acetic acid, propionic acid, and butyric acid to maintain intestinal homeostasis. These findings suggest the potential of DOO as a therapeutic agent for ulcerative colitis (UC).
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