Our data showed that AFC1 compound inhibited the production of ROS, the infiltration of inflammatory cells, as well as the content of inflammatory cytokines, such as IL-1β, TNF-α, and IL-6 in infarcted myocardium, which implied that AFC1 compound may play an important role in improving ventricular remodeling after MI/R via suppressing oxidative stress and inflammatory responses. This evidence concerns the gene IL1B and myocardial infarction.