Tailored Porous Bimetallic Nanozyme Platform for Full‐Cycle Therapeutics of Intestinal Ischemia/Reperfusion

cells) by 96 h. Transcriptomic and immunohistochemical analyses identify three key mechanisms underlying this efficacy: (1) inhibition of the NOD-like receptor family pyrin domain-containing 3 (NLRP3)/ cysteinyl aspartate-specific proteinase 1 (caspase-1) pathway to suppress pyroptosis; (2) upregulation of defensin alpha 1 (DEFA1) and desmoglein 1 (DSG1) for epithelial repair; and (3) enhancement of vascular endothelial growth factor (VEGF) and angiotensin-converting enzyme (ACE) expression for vascular regeneration. Overall, MPB@TA-Cu-Ma achieves synchronized, phase-adaptive therapy by disrupting the oxidative-inflammatory-barrier axis through enhanced ROS scavenging, enzyme-mimetic activity, promotion of angiogenesis, and immune modulation, thereby effectively addressing the complex biphasic pathology of intestinal I/R injury.