Peroxisome proliferator-activated receptor-γ (PPAR-γ) is a transcription factor belonging to the nuclear receptor superfamily that binds to specific response elements. Rosiglitazone, promotes insulin sensitization and is a synthetic agonist ligand of PPAR-γ.1 In recent years, a number of studies have shown that triglitazone and piglitazone, which are chemically related to rosiglitazone, can attenuate postinfarction left ventricular remodeling,2 but there are few studies assessing whether rosiglitazone similarly improves postinfarction left ventricular remodeling and cardiac function. Therefore, the purpose of this study was to determine whether rosiglitazone can improve left ventricular remodeling and cardiac function in a rat model of post-myocardial infarction (MI), and to explore potential underlying mechanisms.