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 Nav1.5 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 Nav1.5dose-dependently with an IC50 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 Nav1.5dose-dependently with an IC50 of 24.0 ± 2.4 mg/mL.
Highlights
Cardiac arrhythmia is a group of conditions in which the heart beats irregularly [1]
Compared with the control group, in the same manner, Dingji Fumai decoction (DFD) and metoprolol prolonged the occurrence of arrhythmia. e time did not show any significant alteration between the DFD group and the metoprolol group (Figure 1(f ))
In the ECG study, we found that DFD prolonged the occurrence and shortened the duration of ventricular arrhythmia (VA) in rats with VA induced by barium chloride and aconitine. erefore, we deduced that DFD may be related to inward rectifier potassium channel, and it can prevent and postpone arrhythmia by promoting K+ outflow and reducing intracellular positive potential and automaticity
Summary
Cardiac arrhythmia is a group of conditions in which the heart beats irregularly [1]. Dingji Fumai decoction (DFD) is an empirical prescription developed by Professor Luo, a national tutor, according to the basic theory of traditional Chinese medicine for the treatment of palpitation ( known as arrhythmia in modern medicine). We report the effect of DFD on the electrocardiogram (ECG) of rats with barium chloride- and aconitine-induced VA, antioxygen free radical, Na+-K+-ATPase and connexin-43 (Cx43), and Nav1.5 sodium channel to elicit the antiarrhythmic. Dingji Fumai decoction (DFD) is used to treat ventricular arrhythmia, and it has provided a very good curative effect. Electrocardiogram was recorded, and oxidative stress response and ion-channel-related molecules were detected in rats with barium chloride- and aconitine-induced ventricular arrhythmia. E 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 Nav1.5dose-dependently with an IC50 of 24.0 ± 2.4 mg/mL Conclusions. e 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 Nav1.5dose-dependently with an IC50 of 24.0 ± 2.4 mg/mL
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