Abstract: Ulcerative colitis (UC) is a chronic inflammatory bowel disease triggered by multiple factors, characterized by gut microbiota dysbiosis, epithelial barrier dysfunction, and abnormal mucosal immunity. Aryl hydrocarbon receptor (AHR) ligands, including agonists and antagonists, are small molecules that directly bind to AHR, promoting its nuclear translocation and transcriptional regulation of downstream genes. Studies have shown that a long-term deficiency of AHR agonists in the diet can increase the risk of UC. The AHR ligands in foods and their metabolites can regulate the homeostasis of intestinal epithelial and immune cells by modulating AHR signaling, thereby alleviating colonic inflammation. This article summarizes the role of AHR in regulating the key cells of the intestinal barrier in UC and proposes that AHR agonists have cell-specific effects. It outlines the common food sources and metabolic pathways of AHR ligands, as well as food components that can synergistically enhance AHR signaling and the underlying mechanisms. The paper also explains the reasons for the unstable effects of certain AHR ligands, providing a scientific basis for exploring diet-based intervention strategies for UC.

Key words: ulcerative colitis, aryl hydrocarbon receptor, intestinal barrier, immune cells, intestinal epithelial cells