Schematic illustration of BBR@PLGA@PLT NPs for MI therapy. After BBR@PLGA@PLT NPs accumulate in infarcted myocardium via inflammation targeting, PLGA undergoes hydrolysis, and sustained release of BBR begins. A high concentration of BBR in infarcted myocardium promotes macrophage polarization to the M2 phenotype and protects cardiomyocytes