Fig. 6

Therapeutic mechanisms of nanomaterials in the intestine. A In the intestine of IBD patients, inflammatory regions accumulate large amounts of ROS produced by goblet cells (H₂O₂, O₂^·−, ·OH, ¹O₂). This signal activates Toll-like receptor-mediated NF-κB signaling pathway. At the same time, macrophages produce large amounts of TNF-α and activate more monocytes as well as Th1 cells, resulting in large levels of pro-inflammatory factors IL-1β, IL-6, IFN-γ, TNF-α. Nanomaterials with antioxidant effect remove overexpressed ROS and convert them into water and oxygen. Meanwhile, the nano drug delivery system can release anti-inflammatory drugs in a targeted position, which inhibit TNF-α expression and induce Treg cells, Th2 cells to secrete IL-10, IL-25, TGF-β and other anti-inflammatory factors to relieve inflammation. B Mucosal damage is a sign of the intestinal tract in IBD patients. When goblet cells secrete insufficient amounts of AMP, MUC, the mucosal layer border is thinned or gapped. Pathogenic bacteria and their product LPS cross the mucosal barrier to induce an innate immune response. Immune cells such as dendritic cells produce pro-inflammatory factors IFN-γ and IL-6 in response to the inflammatory environment, resulting in mislocalization and reduced expression of tight junction proteins, further weakening the function of the intestinal mucosal barrier. Related functional nanomaterials or drug delivery systems increase the relative abundance of probiotics and contribute to the recovery of the mucosa and mucus layer by upregulating the expression of tight junction proteins (ZO-1, Occludin, Claudin). IL-1β interleukin-1β, IL-6 interleukin-6, ΝF-κB nuclear factor-κB, TNF-α tumour necrosis factor α, IL-10 interleukin-10, IL-25 interleukin-25, AMP antimicrobial peptide, MUC mucin, IFN-γ interferon-γ, TGF-β transforming growth factor-β