Nutritional trace elements influence the pathogenesis and resolution of inflammatory bowel disease

Inflammatory bowel disease (IBD) is a chronic intestinal inflammatory condition driven by a combination of genetic, environmental, and immune factors. This review systematically explores the roles of selenium, copper, zinc, iron, and magnesium, five key trace elements, in the pathogenesis, disease progression, and potential treatment of IBD. These elements profoundly affect the pathological state of IBD by regulating oxidative stress, immune cell function (such as macrophage polarization, Th17/Treg balance), intestinal epithelial barrier integrity, and gut microbiota composition. For example, selenium deficiency exacerbates inflammation, while selenium supplementation can alleviate the condition; copper homeostasis imbalance participates in the disease through oxidative stress and the emerging "cuproptosis" pathway; zinc deficiency destroys the barrier and enhances the IL-23/Th17 axis to drive inflammation; iron metabolism disorder leads to anemia and regulates the ferroptosis process; magnesium maintains the barrier through the TRPM6 channel and affects the abundance of probiotics. In recent years, nanomaterials based on these elements (such as nanoselenium, copper/zinc complexes, iron-based nanoenzymes, etc.) have shown great potential as novel therapeutic strategies. They effectively alleviate colitis in preclinical models by enhancing targeting, improving bioavailability, and synergistically exerting antioxidant and anti-inflammatory effects. However, current research is mostly limited to the preclinical stage, and its clinical translation faces challenges such as optimal dosages, long-term safety, interactions between elements, and individual differences. In summary, restoring and maintaining trace element balance is a promising auxiliary strategy in the management of IBD. Future research should focus on developing intelligent delivery systems, combining personalized nutrition and medicine, to promote the transformation of trace elements from basic nutritional support to mechanism-driven, precise auxiliary treatment, ultimately improving the long-term prognosis of IBD patients.