Clinical evidence has indicated an increased myocardial infarction (MI) morbidity and mortality after exposure to air pollution (particulate matter<2.5 mu m PM2.5). However, the mechanisms by which PM2.5 aggravates MI remain unknown. Present study was to explore the adverse effect of PM2.5 on myocardium after MI and the potential mechanisms. Male mice with MI surgery were treated with PM2.5 by intranasal instillation. Neonatal mice ventricular myocytes (NMVMs) subjected to hypoxia were also incubated with PM2.5 to determine the role of PM2.5 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 BCI-2 indicated that PM2.5 exposure could cause cellular apoptosis in vivo and in vitro. Besides, PM2.5 activated NF kappa B pathway and increased gene expression of IL-1 beta and IL-6 in NMVMs with hypoxia, which could be effectively reversed by SN-50-induced blockade of NF kappa B trans location to the nucleus. In summary, air pollution induces myocardium apoptosis and then impairs cardiac function and aggravates MI via NF kappa B activation. (C) 2017 Elsevier Inc. All rights reserved.