We provide evidence for the following: (1) SA increased M2 macrophage infiltration in the peripheral infarct zones after MI; (2) SA attenuated myocardial interstitial fibrosis and neural remodeling after MI; (3) SA induced and promoted macrophage M2 polarization in BMDMs and IL-4-treated BMDMs in vitro; and (4) activation of PPARγ is a potential mechanism by which SA regulates macrophage polarization. This evidence concerns the gene PPARG and myocardial infarction.