In the rat model of myocardial ischemia/reperfusion injury, Tilianin could improve mitochondrial energy metabolism through AMPK/SIRT1/PGC-1α signaling, attenuate oxidative stress, significantly decrease the level of ROS and MDA, markedly alleviate myocardial infarction, evidently enhance myocardial pathological morphology, and reduce myocardial ischemia/reperfusion injury [39]. This evidence concerns the gene PRKAA1 and myocardial ischemia.