Fig. 4. Effects of protopanaxadiol (PPD) on Rg3-mediated IHERG, Itail, and Ideactivating-tail. (A) Representative current traces on human ether-a-go-go-related gene (HERG) K+ channel inhibitions by various concentrations of PPD itself (left panel). Currents were in response to 4-s voltage steps to 0 mV from a holding potential of –90 mV, followed by repolarization to –60 mV. IHERG was obtained at the end of depolarization; Itail was obtained at beginning of repolarization; slow Ideactivating-tail was obtained at the end of repolarization as indicated by the arrow. Concentration-dependent inhibitions of HERG K+ currents by PPD on Rg3-mediated IHERG, Itail, and Ideactivating-tail (right panel). (B) I-V relationships for HERG K+ currents measurement at the end of the 4-s test pulse before (upper traces) and after application of 1 μM Rg3 plus 100 μM PPD (down traces). Currents were normalized to the control current at 0 mV for each oocyte (right panel). Data are represented by the means±SEM (n=7). (C) Concentration-response curves for the activation of HERG K+ currents by Rg3 in the absence or presence of PPD on IHERG, Itail, and Ideactivating-tail. Solid lines were fitted to the Hill equation. PPD significantly affected Ideactivating-tail. Bars represent the means±SEM (n=5-7). (D) Effects of PPD on Rg3-mediated the steady-state activation curve for HERG K+ channel. Itail were normalized to the peak current under each condition, and the data were fitted with a Boltzmann function. Treatment of 100 μM PPD in the presence of 0.3, 1, or 3 μM Rg3 did not cause a leftward shift. Con, control.
