D-Tagatose attenuates DSS-induced ulcerative colitis by inhibiting inflammation, reducing intestinal barrier damage and modulating the intestinal flora composition.

Ulcerative colitis (UC) is a prevalent inflammatory bowel disease (IBD) posing a significant health threat. This study explored the protective effects of D-tagatose against DSS-induced colitis in mice and its underlying mechanisms using H&E staining, AB-PAS staining, immunofluorescence, immunohistochemistry, ELISA, qPCR, western blotting, and other assays. D-Tagatose improved colitis by increasing body weight and colon length, with decreased DAI (disease activity index) and histopathological scores. The results showed that D-tagatose inhibited the secretion of myeloperoxidase (MPO), inflammatory enzymes (iNOS and COX-2) and pro-inflammatory cytokines (TNF-α, IL-1β and IL-6) as well as increased the content of anti-inflammatory cytokines (IL-10) in vitro. In addition, D-tagatose enhanced the expression of tight junction proteins (ZO-1 and Occludin) and mucin (MUC-2). Furthermore, D-tagatose was able to modulate the gut microbiota dysbiosis caused by DSS-induced UC and increased the content of short-chain fatty acids (SCFAs). This study indicated that D-tagatose attenuated DSS-induced UC by modulating inflammatory cytokines, restoring intestinal barrier function, maintaining gut microbiota homeostasis, and enhancing SCFA production. These findings provide D-tagatose as a safe and effective novel functional food strategy for the prevention and treatment of UC.