SOD2 and myocardial infarction: Subsequently, an acacetin phosphate prodrug was applied to the in vivo experiments of ischemia/reperfusion injury, and the studies showed that acacetin inhibited the apoptosis of myocardial cells by preventing the reduction of antioxidants such as SOD-2 and thioredoxin and reducing the release of inflammatory cytokines such as TLR4, IL-6, and TNFα, thus playing a protective role on the myocardium after myocardial infarction (MI) [34].