Alginate oligosaccharides

Alginate oligosaccharide (AOS) is a structurally distinct carbohydrate derived from marine algae. In this study, AOS was obtained through the enzymatic hydrolysis of alginate, and the anti-inflammatory efficacy of AOS was assessed in lipopolysaccharide (LPS)-induced inflammatory Balb/c mice. AOS effectively suppressed the overexpression of TNF-α, IL-6, and MDA while restoring the reduced SOD activity. Histopathological analysis revealed that AOS significantly reduced the level of LPS-induced tissue edema, inflammatory infiltration, and villous destruction. Additionally, AOS notably upregulated tight junction proteins Claudin-1, Occludin, and ZO-1 expression. Transcriptomic and Western blot analyses indicated that AOS primarily mediated the restriction of the TLR4/MAPK/NF-κB pathway in the jejunum. Moreover, AOS ameliorated gut microbiota dysbiosis, such as increasing in Bacteroidota, alongside decreasing in Firmicutes, Campylobacter, and Desulfovibrio, respectively. Metabolomics demonstrated that AOS improved the LPS-induced reduction of short-chain fatty acids in the gut. These results provide compelling evidence supporting the potential of AOS against acute intestinal inflammation.

Alginate oligosaccharides (AOS) have gained attention for their capacity to regulate human health as prebiotics. Osteosarcopenia is a progressive disease of the musculoskeletal system and result in heavy burden of patients. Studies suggest that gut microbiota is involved in the pathogenesis of osteosarcopenia, whether AOS can improve the symptoms of osteosarcopenia by modulating gut microbiota remains to be elucidated. In this study, we proved that 200 mg/kg body weight AOS (MW = 4.9 kDa, G/M = 1.88) treatment significantly increased bone mass, boosted muscle function, and promoted gut barrier integrity in ovariectomized (OVX) mice. After AOS treatment, a marked reduction in the proportion of intestinal Th17 subsets and in peripheral levels of relevant inflammatory cytokines was observed compared to the OVX group. 16S rRNA sequencing indicated that AOS treatment could restore the imbalance of gut microbiota caused by estrogen deficiency. Additionally, the impact of AOS on bile acid changes was revealed according to metabolomics. In particular, the Th17 differentiation inhibitor, such as isoLCA, were significantly upregulated after AOS treatment. In conclusion, AOS can alleviate the symptoms of osteoporosis by modulating the relative abundance of gut microbiota and bile acid metabolism, thereby reducing the proportion of intestinal Th17 cells and peripheral Inflammation.