Abstract
BACKGROUND: Dingji Fumai decoction (DFD) is used to treat ventricular arrhythmia, and it has provided a very good curative effect. However, its cellular electrophysiological mechanism is unknown. METHODS: Electrocardiogram was recorded, and oxidative stress response and ion-channel-related molecules were detected in rats with barium chloride- and aconitine-induced ventricular arrhythmia. Moreover, whole-cell patch-clamp assay was used to investigate the inhibitory effect of DFD on Nav(1.5) in Chinese hamster ovary cells. RESULTS: DFD prolonged the occurrence time and shortened the duration of ventricular arrhythmia, decreased the malondialdehyde and increased the superoxide dismutase, and alleviated the activation of Na(+)-K(+)-ATPase and connexin-43. DFD suppressed Nav(1.5)dose-dependently with an IC(50) of 24.0 ± 2.4 mg/mL. CONCLUSIONS: The clinical antiarrhythmic mechanisms of DFD are based on its antioxidant potential, alleviation of Na(+)-K(+)-ATPase and connexin-43, and class I antiarrhythmic properties by suppressing Nav(1.5)dose-dependently with an IC(50) of 24.0 ± 2.4 mg/mL.