Ginsenoside Rg1 exerts anti-arrhythmic effect by inhibiting ICaL through cAMP-PKA and PI3K-AKT signaling pathways in rat ventricular myocytes after myocardial ischemia-reperfusion injury.

ObjectiveGinsenoside Rg1 has demonstrated beneficial effects in myocardial ischemia-reperfusion (I/R) injury. However, its potential anti-arrhythmic role in ventricular arrhythmias remains unclear.MethodsIn this study, a whole-cell patch clamp technique was employed to evaluate the effects of Rg1 on L-type calcium current (ICaL) and ventricular arrhythmia. Western blot analysis was conducted to investigate the underlying signaling pathways involved.ResultsGinsenoside Rg1 inhibited ICaL in ventricular myocytes in a concentration-dependent manner. Additionally, Rg1 alleviated the I/R-induced increase in diastolic intracellular calcium concentration ([Ca2+]i) and reduced calcium overload. Importantly, Rg1 decreased the incidence of ventricular tachycardia (VT) and ventricular fibrillation (VF) in I/R injury models. Mechanistically, these cardioprotective effects appear to be mediated via modulation of the cAMP-PKA and PI3K-AKT signaling pathways.ConclusionsRg1 may attenuate the deterioration of cardiac function during acute I/R injury, lower the susceptibility to ventricular arrhythmias, and prevent their occurrence following I/R. These findings suggest that Rg1 holds therapeutic potential in the management of I/R-induced ventricular arrhythmias.