Naringin is a flavonoid extracted from citrus plants which have a variety of biological activities. Studies have shown that eating more food rich in flavonoids can reduce the incidence of cardiac arrhythmia. Naringin has been reported to have beneficial cardiovascular effects but its electrophysiological mechanism against arrhythmia has not been elucidated. Here, we used the whole-cell patch-clamp technique and BL-420F biological signal acquisition and analysis system to record the APs, ionic currents, and Electrocardiogram (ECG). At the cellular level, naringin prolonged the APD of ventricular myocytes and decreased the Vmax of APs. Naringin inhibited L-type calcium current (ICa.L), peak sodium current (INa.P), delayed rectifier potassium current (IK), transient outward potassium current (Ito), and ATX II enhanced late sodium current (INa.L) in a concentration-dependent manner. Moreover, naringin reduced CaCl2-induced DADs and ATX II-induced APD prolongation and EADs. At the organ level, naringin reduced the incidence of VT and VF induced by ATX II and prolonged the onset time of both in mouse hearts. For the first time, the electrophysiological method was applied to elucidate that naringin may be a multi-channel blocker with antiarrhythmic effects.