Bovine lactoferrin improves doxorubicin- and ischemia-reperfusion-induced myocardial injury by activating AMPK-mediated signaling pathways

Doxorubicin- (DOX) and ischemia-reperfusion (I/R)-induced acute myocardial injury pose a serious threat to human health and have brought a heavy medical and social burden. Currently, specific therapeutic drugs for the clinical treatment of myocardial injury induced by DOX or I-R are still lacking. Based on this, this study focuses on the potential of lactoferrin (LF) in treating myocardial injury. To further investigate the specific effects of LF on myocardial injury caused by I/R and DOX, a series of biochemical experiments were performed. We found that LF can effectively alleviate the myocardial cell damage caused by DOX and I/R. The experimental data showed that LF alleviated the cell proliferation inhibition, inflammation, oxidative stress, aging, and other related damages caused by DOX or I/R. Further mechanistic studies showed that LF exerts its myocardial protective effect by inhibiting the ferroptosis pathway and activating the AMPK-mediated signaling pathway. In the in vivo model, the corresponding experimental results also showed that LF could significantly improve the myocardial injury mediated by DOX and I/R. In summary, this study shows that LF has significant therapeutic effects in improving I/R- and DOX-induced myocardial injury. This finding establishes a crucial research foundation for elucidating the biological functions of LF.