GSH-derived carbon dot-mediated interfacial electron transfer modulates pH-Dependent redox catalysis of Ce-MOF nanozymes for wound healing.

Infected wounds require therapeutic materials that can control bacterial infection without aggravating oxidative tissue damage. Here, glutathione-derived carbon dots (GSH-CDs) were introduced during the formation of a cerium metal-organic framework (Ce MOF) through an in situ integration strategy to construct a carbon-dot-integrated Ce MOF nanozyme (Ce MOF-CD). Electronic-structure analyses supported interfacial electron redistribution from GSH-CDs toward Ce MOF, accompanied by changes in the local electronic environment and Ce3+/Ce4+ distribution of the Ce active centers. Ce MOF-CD exhibited a distinct pH-dependent redox catalytic preference, with oxidase-like catalysis favored under acidic conditions and superoxide dismutase-like activity becoming more pronounced near neutrality. Accordingly, Ce MOF-CD markedly reduced the viability of MRSA and E. coli and disrupted established biofilms under acidic conditions. Under near-neutral cellular conditions, it reduced intracellular oxidative stress, attenuated inflammatory activation, and promoted repair-associated macrophage polarization. In an MRSA-infected wound model, Ce MOF-CD reduced bacterial burden and local inflammation, promoted tissue reconstruction, and accelerated wound closure with favorable biosafety. Overall, GSH-CDs-mediated interfacial electronic regulation modulates the pH-dependent redox catalytic behavior of Ce MOF, enabling antibacterial activity to be coordinated with oxidative-stress regulation during infected wound healing.