Acute　kidney　injury　(AKI)　has　a　very　high　incidence　in　hospitalized　patients,　but　it　lacks　effective　therapy　clinically.　Its　pathogenesis　is　associated　with　capillary　hypoperfusion　around　renal　tubules,　production　of　reactive　oxygen　free　radicals　(ROS),　and　infiltration　of　inflammatory　cells.　Endogenous　carbon　monoxide　(CO)　can　protect　cells　or　organs　by　vasodilation,　anti-inflammation,　and　reducing　oxidative　stress　injury.　However,　direct　exogenous　CO　supplementation　is　difficult　to　control　the　exact　dose,　and　excessive　CO　has　obvious　toxicity,　which　is　difficult　to　be　applied　in　clinical　treatment.　In　this　study,　we　constructed　H2O2-responsive　nanomedicine　for　CO　therapy　of　AKI　by　loading　manganese　carbonyl　(MnCO)　onto　the　hollow　mesoporous　silicon　nanoparticles　(hMSN),　which　were　coated　with　a　neutrophil　membrane　with　the　insertion　of　phosphatidylserine　(PS)　into　the　membrane　surface　(MnCO@hMSN@NM-PS).　MnCO@hMSN@NM-PS　was　located　in　the　renal　tubules　of　AKI　through　the　biomimetic　chemotaxis　of　the　neutrophil　membrane　to　the　inflammation　site　and　the　active　binding　of　PS　to　kidney　injury　molecule-1　(KIM-1),　which　was　overexpressed　in　damaged　renal　tubular　epithelial　cells.　MnCO@hMSN@NM-PS　had　a　good　protective　effect　on　oxidative　damage　of　renal　tubular　cells　in　vitro　and　glycerol-induced　AKI　in　vivo.　MnCO@hMSN@NM-PS　offers　hope　for　the　treatment　of　AM.