Leucrose, a natural sucrose isomer, suppresses dextran sulfate sodium (DSS)-induced colitis in mice by regulating macrophage polarization via JAK1/STAT6 signaling

The purpose of the present study was to investigate the anti-inflammatory effects of a sugar isomer, leucrose (D-glucopyranosyl-alpha-(1-5)-D-fructopyranose) in a dextran sulfate sodium (DSS)-induced colitis mouse model and in RAW 264.7 macrophages. Colitis was induced in vivo with administration of two cycles of DSS (2.5%). Two groups of mice received an AIN-93G diet with 25% or 50% of the total sucrose content replaced with leucrose. This leucrose supplementation improved disease activity index (DAI) scores, colon length, histopathological damage, and myeloperoxidase (MPO) activity levels. In addition, the expression of pro-inflammatory mediators and cytokines decreased in the leucrose supplementation groups compared with the DSS alone treatment group. Furthermore, leucrose supplementation increased M2 macrophage polarization. Leucrose treatment suppressed IL-4-induced M2 polarization and increased JAK1/STAT6 phosphorylation in RAW264.7 cells. Taken together, these results indicate that leucrose exerts an anti-inflammatory effect by regulating M2 macrophage polarization via inflammatory cytokines and the JAK1/STAT6 signaling pathway.