Exposure to particulate matter induces cardiomyocytes apoptosis after myocardial infarction through NFκB activation

Abstract Clinical evidence has indicated an increased myocardial infarction (MI) morbidity and mortality after exposure to air pollution (particulate matter in vitro . Exposure to PM2.5 significantly impaired the cardiac function and increased the infarct size in MI mice. TUNEL assay, flow cytometry and western blotting of Caspase 3, Bax and BCl-2 indicated that PM2.5 exposure could cause cellular apoptosis in vivo and in vitro . Besides, PM2.5 activated NFκB pathway and increased gene expression of IL-1β and IL-6 in NMVMs with hypoxia, which could be effectively reversed by SN-50-induced blockade of NFκB translocation to the nucleus. In summary, air pollution induces myocardium apoptosis and then impairs cardiac function and aggravates MI via NFκB activation.