Inflammatory bowel disease (IBD), which includes Crohn’s disease (CD) and ulcerative colitis (UC), can affect the entire gastrointestinal tract and mucosal layer and lead to intestinal damage and intestinal dysfunction. IBD is an inflammatory disease of the gastrointestinal tract that significantly impacts public health development. Monoclonal antibodies and other synthetic medications are currently used to treat IBD, but they are suspected of producing serious side effects and causing a number of other problems with long-term use. Numerous in vitro and in vivo studies have shown that organic macromolecules from plants and animals have an alleviating effect on IBD-related problems, and many of them are also capable of altering enzymatic function, reducing oxidative stress, and inhibiting the production of cytokines and release of proinflammatory transcriptional factors. Thus, in this paper, the natural products with potential anti-IBD activities and their mechanism of action were reviewed, with a focus on the protective effects of natural products on intestinal barrier integrity and the regulation of tight junction protein expression and remodeling. In conclusion, the insights provided in the present review will be useful for further exploration and development of natural products for the treatment of IBD.

As one of the most representative natural products among flavonoids, quercetin (QUE) has been reported to exhibit beneficial effects on gut health in recent years. In this study, we utilized a dextran sulfate sodium (DSS)-induced colitis mice model to explore the protective effects and underlying mechanisms of QUE on colitis. Our data demonstrated that QUE oral gavage administration significantly ameliorates the symptoms and histopathological changes associated with colitis. Additionally, the concentration of mucin-2, the number of goblet cells, and the expression of tight junction proteins (such as ZO-1, Occludin, and Claudin-1) were all found to be increased. Furthermore, QUE treatment regulated the levels of inflammatory cytokines and macrophage polarization, as well as the oxidative stress-related pathway (Nrf2/HO-1) and associated enzymes. Additionally, 16S rDNA sequencing revealed that QUE treatment rebalances the alterations in colon microbiota composition (inlcuding Bacteroidaceae, Bacteroides, and Odoribacter) in DSS-induced colitis mice. The analysis of network dynamics reveals a significant correlation between gut microbial communities and microenvironmental factors associated with inflammation and oxidative stress, in conjunction with the previously mentioned findings. Collectively, our results suggest that QUE has the potential to treat colitis by maintaining the mucosal barrier, modulating inflammation, and reducing oxidation stress, which may depend on the reversal of gut microbiota dysbiosis.