Intestinal epithelial barrier dysfunction with dysbiosis of gut microbiota contributes to the occurrence and acceleration of colitis. This study aimed to evaluate the effect of flaxseed oligosaccharides (FOSs) on dextran sulfate sodium (DSS)-induced ulcerative colitis (UC) mice and to elucidate the underlying mechanisms. UC was induced in mice by administering 2% DSS in drinking water for 8 days. Then, FOS (50 mg kg⁻¹ d⁻¹, 100 mg kg⁻¹ d⁻¹ and 200 mg kg⁻¹ d⁻¹) was administered by gavage for 14 days. The results showed that FOS treatment (200 mg kg⁻¹ d⁻¹) significantly ameliorated colitis by decreasing disease activity index (DAI), increasing colon length and improving colonic histology. FOS treatment (200 mg kg⁻¹ d⁻¹) down-regulated the critical markers of oxidative stresses, including malondialdehyde (MDA) and myeloperoxidase (MPO). Furthermore, FOS (200 mg kg⁻¹ d⁻¹) significantly suppressed the levels of pro-inflammatory cytokines including tumor necrosis factor (TNF)-α, interleukin (IL)-6 and interleukin (IL)-1β but increased that of anti-inflammatory cytokine interleukin (IL)-10. The 16S rDNA gene high-throughput sequencing results indicated that FOS treatment increased the gut microbial diversity and inhibited the proliferation of inflammation-related bacteria such as unidentified_Clostridiales. An increase in total short-chain fatty acids (SCFAs), propionic acid and butyric acid, was also observed by FOS supplementation. FOS (200 mg kg⁻¹d⁻¹) also protected the intestinal barrier by increasing the protein levels of Claudin1 and Occludin. In conclusion, FOS attenuated DSS-induced colitis by modulating the gut microbiota and repairing the intestinal barrier.

The digestion of flaxseed polysaccharides (FSP) in simulated saliva, gastric and small intestine conditions was assessed, as well as in vitro fermentation of FSP by human gut microbiota. FSP was not degraded in the simulated digestive systems (there was no change in molecular weight or content of reducing sugars), indicating that ingested FSP would reach the large intestine intact. Changes in carbohydrate content, reducing sugars and culture pH suggested that FSP could be broken down and used by gut microbiota. FSP modulated the composition and structure of the gut microbiota by altering the Firmicutes/Bacteroidetes ratio and increasing the relative abundances of Prevotella, Phascolarctobacterium, Clostridium and Megamonas, which can degrade polysaccharides. Meanwhile, FSP fermentation increased the concentration of short-chain fatty acids, especially propionic and butyric acids. Our results indicate that FSP might be developed as a functional food that benefits gut health.

Algal oil is rich in docosahexaenoic acid (DHA) and has various health benefits against human metabolic disorders and disease. This study aimed to investigate the effects of DHA algal oil on colonic inflammation and intestinal microbiota in dextran sulfate sodium (DSS)-induced colitis mice model. Male C57BL/6 mice was induced colitis by 2.5% DSS and followed by 2 weeks of treatment with algal oil (250 or 500 mg/kg/day). The colonic inflammation was assessed by colon macroscopic damage scores, and the degree of neutrophil infiltration was evaluated by measuring tissue-associated myeloperoxidase (MPO) activity in colonic mucosa. Tight junction proteins in the colonic tissue were measured by real-time PCR and western blot. Moreover, the intestinal microbiota and shot chain fatty acids (SCFAs) were estimated by bioinformatic analysis and GC, respectively. Colonic damage due to DSS treatment was significantly ameliorated by algal oil supplementation. In addition, algal oil significantly inhibited the increases of malondialdehyde (MDA) content, MPO activity, pro-inflammatory cytokines level and tight junction proteins expression in DSS-treated mice. Furthermore, supplementation of algal oil modulated the intestinal microbiota structure in DSS induced colitis mice by increasing the proportion of the unidentified_S24_7 and decreasing the relative abundance of unidentified_Ruminococcaceae, Clostridium and Roseburia. On the analysis of SCFAs, the caecal content of acetic acid, propionic acid, isobutyric acid, buturic, and the total SCFAs showed a significant increase in algal oil-administered mice. Together, these results suggested that algal oil rich in DHA inhibited the progress of DSS-induced colitis in mice by modulating the intestinal microbiota and metabolites and repairing the intestinal barrier, which may be applied in the development of therapeutics for intestinal inflammation.