The clinically restored blood supply post myocardial infarction (MI) will break the physiological and metabolic balance of the ischemic myocardial region, leading to a new injury known as myocardial ischemia/reperfusion (I/R) injury. Abundant oxygen brought by the fresh blood would trigger the damaged myocardium to produce excessive reactive oxygen species (ROS) and thereby inflammation along with the recruitment and infiltration of activated neutrophils and macrophages. Inspired by the active targeting process of inflammatory cells, a novel "neutrophil-like" nanoassembly (At@NQA) was prepared by modifying neutrophil membrane fragments onto At@QA NPs containing 1:1 (molar ratio) calixarene molecule (QA) and anti-inflammatory and anti-fibrotic atorvastatin calcium (At). Tail vein injection of the At@NQA could efficiently target the damaged myocardium, inhibit oxidative damage and inflammation, reduce myocardial fibrosis, increase myocardial troponin T (cTnT) and connexin 43 (Cx43) expression, and thus improve cardiac functions effectively.