Abstract
Baicalin is a natural flavonoid glycoside that confers protection against myocardial ischemia/reperfusion (I/R) injury. However, its mechanism has not been fully understood. This study focused on elucidating the role of ferroptosis in baicalin-generated protective effects on myocardial ischemia/reperfusion (I/R) injury by using the myocardial I/R rat model and oxygen–glucose deprivation/reoxygenation (OGD/R) H9c2 cells. Our results show that baicalin improved myocardial I/R challenge–induced ST segment elevation, coronary flow (CF), left ventricular systolic pressure , infarct area, and pathological changes and prevented OGD/R-triggered cell viability loss. In addition, enhanced lipid peroxidation and significant iron accumulation along with activated transferrin receptor protein 1 (TfR1) signal and nuclear receptor coactivator 4 (NCOA4)-medicated ferritinophagy were observed in in vivo and in vitro models, which were reversed by baicalin treatment. Furthermore, acyl-CoA synthetase long-chain family member 4 (ACSL4) overexpression compromised baicalin-generated protective effect in H9c2 cells. Taken together, our findings suggest that baicalin prevents against myocardial ischemia/reperfusion injury via suppressing ACSL4-controlled ferroptosis. This study provides a novel target for the prevention of myocardial ischemia/reperfusion injury.
Highlights
Acute myocardial infarction (AMI), which arises from thrombotic occlusion of a coronary artery, is a major cause of global morbidity and mortality (Roger et al, 2012)
Iron Accumulation Since ferroptosis is an iron-dependent cellular death, we investigated whether baicalin could render iron accumulation in rats exposed to myocardial I/R surgery
Previous studies suggest that various mechanisms are implicated in baicalin-induced beneficial effects in myocardial ischemia/reperfusion injury (Bai et al, 2019; Luan et al, 2019)
Summary
Acute myocardial infarction (AMI), which arises from thrombotic occlusion of a coronary artery, is a major cause of global morbidity and mortality (Roger et al, 2012). The current strategies for AMI treatment focus on percutaneous coronary intervention, which rapidly restores the coronary artery blood flow This could trigger profound myocardial ischemia/reperfusion injury such as myocardial cell death and deterioration of cardiac function (Liang et al, 2017). Ferroptosis is a type of “programmed necrosis” driven by the accumulation of cellular reactive oxygen species (ROS) when the glutathione (GSH)-dependent lipid peroxide repair systems are compromised (Cao and Dixon, 2016). It is characterized by iron dependency and Baicalin Prevented Myocardial Ischemia/Reperfusion lipid peroxides accumulation. Previous studies indicate that ACSL4 is essential for ferroptosis induction, and ACSL4 inhibition can prevent ferroptosis (Doll et al, 2017; Li Y. et al, 2019)
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