Effects of dietary supplementation of glucosamine sulfate on intestinal inflammation in a mouse model of experimental colitis

Background and Aim Epidemiological evidences suggested an inverse association between the use of glucosamine supplements and colorectal cancer ( CRC ) risk. In this study, the efficacy of glucosamine to attenuate dextran sodium sulfate ( DSS )‐induced colitis, a precancerous condition for CRC , was evaluated. Methods C 57 BL /6 mice were separated into three groups receiving glucosamine sulfate at concentrations of 0, 0.05, and 0.10% (w/w) of AIN ‐93 G diet, respectively for 4 weeks. Colitis was induced by supplying two cycles (5 days per cycle) of 2% DSS in the animals' drinking water. Results Glucosamine supplementation at the level of 0.10% of the diet (w/w) reduced colitis‐associated symptoms as measured by disease activity index ( DAI ). Tumor necrosis factor‐α ( TNF ‐α), interleukin‐1β, and nuclear factor‐kappa B mRNA expression in the colonic mucosa was significantly lower in animals fed 0.10% glucosamine compared with those of the control group. Expression of the tight junction proteins ZO ‐1 and occludin was significantly higher in the 0.10% glucosamine‐supplemented group compared with the other groups. Also, colonic protein expression of lipocalin 2, and serum concentrations of interleukin‐8 and amyloid P component ( SAP ) were significantly reduced in the 0.10% glucosamine‐supplemented group compared with the control group. Conclusion These results suggest that glucosamine attenuates the colitis disease activity by suppressing NF ‐ κB activation and related inflammatory responses.