Dual-metal atom nanozymes (DANs) are frontier nanocatalysts that mimic natural enzymes to regulate the level of reactive oxygen species (ROS) in pathological tissue. However, the construction of DANs is mostly based on trial-and-error strategy rather than rational design due to their ambiguous catalytic mechanism. Herein, a promising strategy to construct highly efficient FeZn-NC DANs by “electron-deficient effect” for ROS scavenging is proposed. Redox-inert Zn-N₄ sites and axial N atom induce electron-deficient Fe sites based on different electronegativity to accelerate catalase (CAT)-like reaction. Besides, FeZn-NC mimics superoxide dismutase (SOD) relying on the cyano-group conjugated with the π-system in the carbon carrier. Enhanced CAT-like activity from Fe sites and SOD-like activity from carbon carriers enabled FeZn-NC more effective in mitigating cellular damage and inducing the phenotypic transformation of macrophages in acute inflammatory wounds. This work establishes more precise structure-activity relationships for CAT and SOD mimics and provides a paradigm for the treatment of inflammation-related diseases by catalytic therapy.

中文翻译：

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缺电效应调节铁-氮-碳纳米酶的过氧化氢酶样活性，用于炎症伤口治疗


双金属原子纳米酶 （DAN） 是前沿纳米催化剂，可模拟天然酶以调节病理组织中活性氧 （ROS） 的水平。然而，由于其催化机制模糊，DANs 的构建大多基于试错策略而不是理性设计。在此，提出了一种很有前途的策略，即通过“缺电子效应”构建高效的 FeZn-NC DAN 用于 ROS 清除。氧化还原惰性 Zn-N₄ 位点和轴向 N 原子基于不同的电负性诱导缺电子 Fe 位点，以加速过氧化氢酶 （CAT） 样反应。此外，FeZn-NC 模拟超氧化物歧化酶 （SOD），依赖于与碳载体中 π 系统偶联的氰基。Fe 位点增强的 CAT 样活性和碳载体的 SOD 样活性使 FeZn-NC 能够更有效地减轻细胞损伤和诱导急性炎症性伤口中巨噬细胞的表型转化。这项工作为 CAT 和 SOD 模拟物建立了更精确的构效关系，并为催化疗法治疗炎症相关疾病提供了范式。