Amorphizing Metal Selenides-Based ROS Biocatalysts at Surface Nanolayer toward Ultrafast Inflammatory Diabetic Wound Healing

The microenvironments with high reactive-oxygen-species (ROS) levels, inflammatory responses, and oxidative-stress effects in diabetic ulcer wounds, leading to poor proliferation and differentiation of stem cells, severely inhibit their efficient healing. Here, to overcome the unbalanced multielectron reactions in ROS catalysis, we develop a cobalt selenide-based biocatalyst with an amorphous Ru@CoSe nanolayer for ultrafast and broad-spectrum catalytic ROS-elimination. Owing to the enriched electrons and more unoccupied orbitals of Ru atoms, the amorphous Ru@CoSe nanolayer-equipped biocatalyst displays excellent catalase-like kinetics (maximal reaction velocity, 23.05 μM s^-1; turnover number, 2.00 s^-1), which exceeds most of the currently reported metal compounds. The theoretical studies show that Ru atoms act as "regulators" to tune the electronic state of the Co sites and modulate the interaction of oxygen intermediates, thus improving the reversible redox properties of active sites. Consequently, the Ru@CoSe can efficiently rescue the proliferation of mesenchymal stem cells and maintain their angiogenic potential in the oxidative stress environment. In vivo experiments reveal the superior ROS-elimination ability of Ru@CoSe on the inflammatory diabetic wound. This study offers an effective nanomedicine for catalytic ROS-scavenging and ultrafast healing of inflammatory wounds and also provides a strategy to design biocatalytic metal compounds via bringing amorphous catalytic structures.