PubMed article abstract display

Abstract

Introduction: Naringin, a flavonoid extracted from citrus plants, has a variety of biological effects. Studies have shown that increasing the consumption of flavonoid-rich foods can reduce the incidence of cardiac arrhythmia. Naringin has been reported to have beneficial cardiovascular effects and thus can be used to prevent cardiovascular diseases, but the electrophysiological mechanism through which it prevents arrhythmias has not been elucidated. This study was conducted to investigate the effect of naringin on the transmembrane ion channel currents in mouse ventricular myocytes and the antiarrhythmic effect of this compound on Langendorff-perfused mouse hearts.

Methods: Action potentials (APs) and ionic currents were recorded in isolated ventricular myocytes using the whole-cell patch-clamp technique. Anemone toxin II (ATX II) and CaCl₂ were used to induce early afterdepolarizations (EADs) and delayed afterdepolarizations (DADs), respectively. Electrocardiogram (ECG) recordings were conducted in Langendorff-perfused mouse hearts with a BL-420F biological signal acquisition and analysis system.

Results: At the cellular level, naringin shortened the action potential duration (APD) of ventricular myocytes and decreased the maximum depolarization velocity (V_max) of APs.Naringin inhibited the L-type calcium current (I_Ca.L) and ATX II enhanced the late sodium current (I_Na.L) in a concentration-dependent manner with IC₅₀ values of 508.5 μmol/L (n = 9) and 311.6 μmol/L (n = 10), respectively. In addition, naringin also inhibited the peak sodium current (I_Na·P) and delayed the rectifier potassium current (I_K) and the transient outward potassium current (I_to). Moreover, naringin reduced ATX II-induced APD prolongation and EADs and had a significant inhibitory effect on CaCl₂-induced DADs as well. At the organ level, naringin reduced the incidence of ventricular tachycardia (VT) and ventricular fibrillation (VF) induced by ATX II and shortened the duration of both in isolated hearts.

Conclusion: Naringin can inhibit the occurrence of EADs and DADs at the cellular level; furthermore, it can inhibit I_Na.L, I_Ca.L, I_Na·P, I_K, and I_to in ventricular myocytes. Naringin also inhibits arrhythmias induced by ATX II in hearts. By investigating naringin with this electrophysiological method for the first time, we determined that this flavonoid may be a multichannel blocker with antiarrhythmic effects.

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