Liquiritigenin protects against myocardial ischemic by inhibiting oxidative stress, apoptosis, and L-type Ca 2+ channels.

Liquiritigenin (Lq) offers cytoprotective effects against various cardiac injuries, but its beneficial effects on myocardial ischemic (MI) injury and the related mechanisms remain unclear. In the in vivo study, an animal model of MI was induced by intraperitoneal injection of isoproterenol (Iso, 85 mg/kg). ECG, heart rate, serum levels of CK and CK-MB, histopathological changes, and reactive oxygen species (ROS) levels were all measured. In vitro, H9c2 cells were divided into four groups and treated for 24 hr with liquiritigenin (30 μmol/L and 100 μmol/L) followed with CoCl 2 (800 μmol/L) for another 24 hr. Cell viability, apoptosis, mitochondrial membrane potential, and intracellular Ca 2+ concentration ([Ca 2+ ] i ) were then assessed. The L-type Ca 2+ current (I Ca-L ) was detected using a patch clamp technique on isolated rat ventricular myocytes. The myocyte contraction and Ca 2+ transients were measured using an IonOptix detection system. The remarkable cardiac injury and generation of intracellular ROS induced by Iso were alleviated via treatment with Lq. CoCl 2 administration induced cell apoptosis, mitochondrial dysfunction, and Ca 2+ overload in H9c2; Lq reduces these deleterious effects of CoCl 2 . Meanwhile, Lq blocked I Ca-L in a dose-dependent manner. The half-maximal inhibitory concentration of Lq was 110.87 μmol/L. Lq reversibly reduced the amplitude of cell contraction as well as the Ca 2+ transients. The results show that Lq protects against MI injury by antioxidation, antiapoptosis, counteraction mitochondrial dysfunction, and inhibition of I Ca-L , thus damping intracellular Ca 2+ .