Liang Bo, Zhou Yan, Fu Ling, Liao Hui-Ling
Nanjing University of Chinese Medicine, Nanjing, China.
Zigong Hospital of TCM, Zigong, China.
Evid Based Complement Alternat Med. 2020 Mar 20;2020:9185707. doi: 10.1155/2020/9185707. eCollection 2020.
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.
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 in Chinese hamster ovary cells.
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 Navdose-dependently with an IC of 24.0 ± 2.4 mg/mL.
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 Navdose-dependently with an IC of 24.0 ± 2.4 mg/mL.
定悸复脉汤(DFD)用于治疗室性心律失常,且已取得很好的疗效。然而,其细胞电生理机制尚不清楚。
记录氯化钡和乌头碱诱导的大鼠室性心律失常的心电图,并检测氧化应激反应和离子通道相关分子。此外,采用全细胞膜片钳技术研究DFD对中国仓鼠卵巢细胞中Nav的抑制作用。
DFD延长了室性心律失常的发生时间,缩短了其持续时间,降低了丙二醛水平,提高了超氧化物歧化酶水平,并减轻了钠钾ATP酶和连接蛋白43的激活。DFD对Nav具有剂量依赖性抑制作用,半数抑制浓度为24.0±2.4mg/mL。
DFD的临床抗心律失常机制基于其抗氧化潜力、对钠钾ATP酶和连接蛋白43的减轻作用以及通过以24.0±2.4mg/mL的半数抑制浓度剂量依赖性抑制Nav而具有的Ⅰ类抗心律失常特性。