Protective effect of edaravone against hypoxia–reoxygenation injury in rabbit cardiomyocytes

We examined whether edaravone (Eda), a clinically available radical scavenger, directly protects cardiomyocytes from ischemia/reperfusion (I/R) injury, and whether the timing of its application is critical for protection. Cardioprotective effects of edaravone were tested in the modified cell‐pelleting model of ischemia and under exogenous oxidative stress (hydrogen peroxide: H2O2) in isolated adult rabbit ventricular cells. Cell death and reactive oxygen species (ROS) generation were detected using propidium iodide (PI) and DCFH‐DA, respectively. These parameters were evaluated objectively using flow cytometory. Hypoxia and reoxygenation aggravated the proportion of dead cells from 32.2±1.8% (Baseline) to 51.3±2.7% (Control). When 15 μM edaravone was applied either throughout the entire experiment (Through) or only at reoxygenation (Reox), cell death was significantly reduced to 39.9±1.8% (P