Abstract

Objective: Dingji Fumai decoction (DFD) is to treat ventricular arrhythmia, we aim to reveal the effect of DFD, which would help to explain the cellular electrophysiological mechanism of DFD. Method: Electrocardiogram was recorded, oxidative stress response and ion channels related molecules were detected in barium chloride and aconitine induced rats with ventricular arrhythmia. Moreover, whole-cell patch clamp assay was used to study the inhibitory effect of DFD on Nav1.5 in CHO cells. Results: DFD prolonged the occurrence time and shortened the duration of ventricular arrhythmia, increased the MDA and decreased the SOD, alleviated the activation of Na+-K+-ATPase and Cx43. The inhibition effect of DFD on Nav1.5 was dose-dependent with an IC50 of 24.0 ± 2.4 g/L. Conclusion: The clinical antiarrhythmic efficacy of DFD is based on its anti-oxygen free radicals and class I antiarrhythmic properties by suppression Nav1.5 dose-dependently with an IC50 of 24.0 ± 2.4 g/L. Funding: This study was conducted as a dissertation for the degree of internal medicine specialist and supported by Sichuan Science and Technology Program (2019YJ0694), Chongqing health and Health Committee (ZY201602167) and Luzhou Science and Technology Program (2016LZXNYD-J09). Declaration of Interest: None. Ethical Approval: All experiments were reviewed and approved by the Committee of Ethics on Animal Experiments and were carried out under the Guidelines for Animal Experiments at the Animal Experiments Center of Southwest Medical University (SCXK2013-17, Luzhou, China).

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