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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 (I Na ) and transient outward potassium channel current (I to ) 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 I Na  and I to  amplitude, while salidroside significantly restored both and altered the I Na  and I to  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.

Effects of Modulation of Ion Channel Currents by Salidroside in H9C2 Myocardial Cells in Hypoxia and Reoxygenation