To address above issues, our present study was designed to (i) characterize the concentration-dependent effects of LLC on the myocardial ischemia injury in vivo and in vitro; (ii) clarify the effects of LLC on the autophagy during myocardial ischemia; and (iii) illuminate whether the PI3K/Akt/mTOR signaling pathway is involved in potential molecular mechanism of LLC-afforded cardioprotection. The gene discussed is AKT1; the disease is myocardial ischemia.