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Effects of Modulation of Ion Channel Currents by Salidroside in H9C2 Myocardial Cells in Hypoxia and Reoxygenation.
Cao, Xue-Bin; Jiang, Zhi-Hao; Dong, Lei; Zheng, Yu; Li, Yang.
Afiliação
  • Cao XB; Department of Cardiology, 252 Hospital of PLA, Baoding, Hebei 071000, China.
  • Jiang ZH; Department of Cardiology, General Hospital of People's Liberation Army, Beijing 100853, China.
  • Dong L; Tianjin University of Traditional Chinese Medicine, Tianjin 300193, China.
  • Zheng Y; State Key Laboratory of Precision Measurement Technology and Instruments, Tianjin University, Tianjin 300072, China.
  • Li Y; Tianjin Key Laboratory of Optoelectronic Detection Technology and Systems, Tianjin Polytechnic University, Tianjin 300387, China.
Article em En | MEDLINE | ID: mdl-30805019
ABSTRACT
Salidroside, a phenyl-propanoid glycoside isolated from the medicinal plant Rhodiola rosea, has potent cardioprotective effects, especially against myocardial hypoxia and reoxygenation injury. However, the molecular mechanism underlying its action is still unclear. The aim of this study was to determine the effect of salidroside on sodium channel current (INa) and transient outward potassium channel current (Ito) in H9C2 cardiomyocytes. H9C2 cells were subcultured under anoxic conditions to mimic myocardial hypoxia and subsequently treated with salidroside. Whole cell patch clamp was performed to determine the effect of hypoxia/reoxygenation and salidroside on myocardial electrophysiological properties. In the differentiated H9C2 cells, hypoxia/reoxygenation reduced INa and Ito amplitude, while salidroside significantly restored both and altered the INa and Ito activation/inactivation kinetics in a dose-dependent manner. Our findings demonstrate that salidroside protects myocardial cells against hypoxia-reoxygenation by restoring the function of sodium and potassium channels.

Texto completo: 1 Base de dados: MEDLINE Idioma: En Ano de publicação: 2019 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Idioma: En Ano de publicação: 2019 Tipo de documento: Article