Xu Xu

This study conducts a structural comparison of alginate-derived oligomannuronic acid (MOS) and its monosaccharide analog, mannose, and evaluates their functional differences in colitis intervention. MOS, an oligosaccharide enzymatically prepared from polymannuronic acid, features a unique C4-C5 double bond at the nonreducing end, distinguishing it from the neutral mannose. Functionally, in vitro experiments showed both MOS and mannose significantly suppressed dextran sulfate sodium induced secretion of proinflammatory cytokines in HCoEpiCs. In addition, they restored tight junction (TJ) integrity by inhibiting the MLCK-MLC2 pathway. In vivo, administration of either compound reduced inflammatory cytokine levels, and enhanced TJ protein expression. Notably, MOS demonstrated superior efficacy over mannose at equivalent or lower doses. Mechanistic studies revealed both agents promoted autophagy and suppressed endoplasmic reticulum stress and apoptosis. These findings underscore the contribution of structural features to the enhanced bioactivity of MOS and support its potential as a polymer-based dietary intervention for inflammatory bowel disease.

This study investigates the protective role of sulfated oligoguluronic acid (SOGA), synthesized from polyguluronic acid (PG)-derived oligoguluronic acid (OGA), against intestinal inflammation and barrier dysfunction. In vitro, SOGA significantly reduced LPS-induced proinflammatory cytokine secretion in THP-1 cells, whereas PG and OGA were ineffective. Mechanistic investigations revealed that SOGA effectively inhibited the activation of LPS-induced NF-κB, JNK MAPK, and NLRP3 inflammasome signaling pathways. In Caco-2 monolayers, SOGA effectively restored mitochondrial function, preserved tight junction integrity, and reduced paracellular permeability. In comparison, this effect was absent for PG and OGA. Additionally, SOGA significantly suppressed the secretion of proinflammatory cytokines in a coculture model of Caco-2/THP-1 cells. In vivo, SOGA ameliorated ulcerative colitis symptoms in mice by reducing inflammation, enhancing tight junction protein expression, and improving mitochondrial function. These findings underscore the potential of SOGA in inflammatory bowel disease treatment by targeting key aspects of inflammation and intestinal barrier dysfunction.

Both enantiomers induced the apoptosis of tumor cells by regulating mRNA expression and activating both extrinsic and intrinsic apoptosis pathways. The higher antitumor efficiency of the Δ-enantiomer should be due to its stronger interaction with DNA.