In DSS-induced mouse colitis models, oral administration of BBR/CUR@MC exerts therapeutic effects through dual mechanisms: on one hand, it regulates TNF signaling pathway targets such as ADAM17 to "top-down" inhibit UC inflammatory cascades; on the other hand, it achieves "full-cycle" antioxidant activity by directly scavenging ROS and inhibiting AGE-RAGE signaling pathway targets such as MAPK11/13. This evidence concerns the gene ADAM17 and colitis.