Effect of puerarin on action potential and sodium channel activation in human hypertrophic cardiomyocytes

Objective: To study the effect of puerarin on electrophysiology using a hypertrophic cardiomyocyte (HC) model. Materials and methods: Human urine epithelial cells were used to generate the HC model (hiPSC-CM). Cardiomyocyte hypertrophy was induced by applying 10 nM endothelin-1 (ET-1). Effects of puerarin pre-treatment (PPr) and post-treatment (PPo) on action potential, sodium current (I(Na)) activation and inactivation, and recovery following I(Na) inactivation were tested using patch clamp electrophysiology. Results: Depolarization to repolarization 50% time (APD50) and repolarization 30% time (APD30) were significantly prolonged in the PPo and PPr groups compared with the controls. However, there were no significant differences in the action potential depolarization amplitude (APA) or the maximum depolarization velocity (V(max)) in phase 0. The PPr group had a slightly shortened APD90, and an extended APD50 and APD30, but did not exhibit any significant changes in stage A of APA and V(max). The PPo group did not exhibit any significant changes in I(Na), while 12 h of PPr improved I(Na). However, puerarin did not significantly affect the activation, inactivation, or recovery of the sodium channel. Conclusions: Cardiomyocyte hypertrophy significantly decreased the V(max) of the action potential and the peak density of I(Na). PPr inhibited the decrease in V(max) and increased the peak density of I(Na). Thus, puerarin could be used to stabilize the electrophysiological properties of hypertrophic cardiomyocytes and reduce arrhythmias.