Tilapia head glycolipids protect mice against dextran sulfate sodium-induced colitis by ameliorating the gut barrier and suppressing NF-kappa B signaling pathway.

The purpose of this study was to evaluate the relieving effect of tilapia head glycolipids (TH-GLs) on dextran sulfate sodium (DSS)-induced colitis in mice and to further explore its mechanism. Mice were orally administered 3% (w/v) DSS to establish a model of ulcerative colitis (UC), and subsequently treated with TH-GLs or sulfasalazine. In addition, the expression of key targets in the intestinal mucosal barrier and the inflammatory signal pathway were studied by combining immunochemical analysis techniques. The results showed that varying doses of TH-GLs can significantly improve colon lesions caused by DSS, reduce histological scores, increase mucus secretion, extend colon length, increase weight, and inhibit the occurrence of inflammatory cytokines such as tumor necrosis factor-α (TNF-α), interferon-γ (IFN-γ), Interleukin-1β (IL-1β), and Interleukin- 6 (IL-6). Further, studies have shown that TH-GLs increase the secretion of MUC2 and up-regulate the expression of tight junction related proteins, such as ZO-1 and Occludin. In addition, TH-GLs significantly down-regulated the protein expression levels of TNF-α, IKK-β, and nuclear factor-κB (NF-κB). Here, we have elucidated the potential mechanism of TH-GLs in protecting mice with colitis. In general, this study shows that TH-GLs could improve the symptoms of UC by improving the gut barrier and inhibiting inflammatory signals, which provides a scientific basis for future clinical applications.