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WEI, H.

Publications and source records attributed to WEI, H..

2 recordsLinked to original sources
bioRxiv2026

Genetically Engineered Biomimetic Nanozymes Reprogram Immune Niches to Intercept Colitis-Carcinoma Transition

Colitis-associated colorectal cancer (CAC) arises from chronic inflammatory niches characterized by persistent oxidative stress and dysregulated immune cell recruitment. Current anti-inflammatory therapies provide only transient symptom relief and fail to prevent malignant progression due to their inability to simultaneously mitigate oxidative injury and immune chemotaxis. Our analysis of clinical samples revealed markedly elevated C-X-C motif chemokine ligand 2 (CXCL2) in intestinal tissues from patients with inflammatory bowel disease (IBD) and CAC, implicating the CXCL2-CXCR2 axis in driving excessive neutrophil and macrophage infiltration and fostering tumorigenesis. Herein, we report a biomimetic nanozymes (PB@ECM) that reprogram inflammatory immune niches to intercept CAC progression. PB@ECM integrates a Prussian blue nanozyme core with genetically engineered macrophage membranes, enabling concurrent scavenging of reactive oxygen species through superoxide dismutase- and catalase-like activities and sequestration of CXCL2 via membrane-displayed CXCR2 receptors. In murine models of colitis and CAC, PB@ECM significantly alleviated intestinal inflammation, suppressed neutrophil and macrophage infiltration, and effectively inhibited colitis-carcinoma transition. By disrupting the pathological crosstalk between oxidative stress and immune chemotaxis, this work establishes a biomimetic nanozyme strategy for preventing inflammation-driven carcinogenesis.

bioengineering↗
bioRxiv2026

Spin-State Modulation by Atom-Cluster Synergy Steers H2O2 Conversion toward a Catalase-like Decomposition Pathway for Anti-Inflammatory Therapy

Nanozymes have emerged as promising enzyme mimics for anti-inflammatory therapy. However, their catalytic efficiency and substrate selectivity generally remain inferior to those of natural enzymes. Single-atom nanozymes (SAzymes), with isolated metal centers resembling enzymatic active sites, represent an important advance toward rational design of nanozyme, but achieving enzyme-like selectivity remains challenging. Herein, we reported a spin-state modulation strategy to prepare Fe-N-C nanozyme with coexisting single atoms and nanoclusters (FeSA+NC) via reductive-gas pyrolysis. Experimental analyses and density functional theory calculations revealed that Fe nanoclusters induced local symmetry breaking and charge redistribution around FeN4 sites, shifting the Fe centers toward a higher spin configuration and thereby modulating the free energy changes of the H2O2 conversion pathway. As a result, FeSA+NC showed dramatically enhanced catalase (CAT)-like activity (333.79 U mg-1) and suppressed peroxidase (POD)-like activity (38.49 U mg-1), achieving superior selectivity compared to Fe SAzymes (FeSA), which showed comparable CAT- and POD-like activities (62.39 and 60.39 U mg-1, respectively). Moreover, FeSA+NC achieved a higher superoxide dismutase (SOD)-like activity (929.27 U mg-1) than FeSA (249.68 U mg-1), enabling efficient SOD-CAT cascade. FeSA+NC effectively scavenged excessive intracellular reactive oxygen species, suppressed M1 macrophage polarization, and enhanced the therapeutic efficacy of intra-articular stem cell injection in a rat model of rheumatoid arthritis, a representative chronic inflammatory disease. This work highlights an atom-cluster synergy strategy for steering H2O2 conversion towards antioxidant pathway, offering a general design principle for safer, more controllable and more efficient nanozyme-based anti-inflammatory therapeutics.

bioengineering↗