Puerarin attenuates myocardial hypoxia/reoxygenation injury by inhibiting autophagy via the Akt signaling pathway

Puerarin (Pur), which is the major bioactive ingredient extracted from the root of Pueraria lobata (Willd.) Ohwi, has been demonstrated to relieve myocardial ischemia/reperfusion (I/R) injury. Macroautophagy, or autophagy, is an evolutionarily conserved cellular catabolic mechanism that is involved in myocardial I/R injury. The present study evaluated the involvement of autophagy in the protective mechanisms of Pur during myocardial hypoxia/reoxygenation (H/R). The results revealed that Pur and 3-methyladenine pretreatment exerted a cardioprotective effect against H/R-induced cell viability loss. Pur also decreased the ratio of light chain 3 (LC3)-II/LC3-I and the degradation of p62 during H/R, which was accompanied by an increased level of phosphorylated-protein kinase B (Akt). These findings suggested that autophagy during myocardial H/R was inhibited by Pur, and this was further confirmed by the results of transmission electron microscopy and adenovirus-monomeric red fluorescent protein-green fluorescent protein-light chain 3 transfection. Furthermore, Pur inhibited the increased levels of autophagy induced by rapamycin, and the autophagy-inhibiting effects of Pur during myocardial H/R were abolished by the Akt signaling inhibitor API-2. Collectively, these data indicate that Pur pretreatment may attenuate myocardial H/R injury by inhibiting autophagy via the Akt signaling pathway.