AIMTo investigate the effect of DSX, an active component extracted from Erigeron breviscapus, on the voltage-gated outward K<sup>+</sup> channel currents in rat retinal ganglion cells (RGCs) by using elect...AIMTo investigate the effect of DSX, an active component extracted from Erigeron breviscapus, on the voltage-gated outward K<sup>+</sup> channel currents in rat retinal ganglion cells (RGCs) by using electrophysiological method, and to explore the possible mechanisms of DSX on optic nerve protection.METHODSOutward K<sup>+</sup> currents were recorded by using whole-cell patch-clamp techniques on acutely isolated rat RGCs. Outward K<sup>+</sup> currents were induced by a series of depolarizing voltage pulses from a holding potential of -70 mV to +20 mV in an increment of 10 mV.RESULTSExtracellular application of DSX voltage-dependently suppressed both the steady-state and peak current amplitudes of outward K<sup>+</sup> currents in rat RGCs. Furthermore, DSX reversibly and dose-dependently inhibited the amplitudes of outward K<sup>+</sup> currents of the cells. At +20 mV membrane potential DSX at the concentrations of 0.02 g/L and 0.05 g/L showed no significant effects on the currents. In contrast, DSX at higher concentrations (0.1 g/L, 0.2 g/L and 0.5 g/L) significantly suppressed the current amplitudes.CONCLUSIONThese results suggest that DSX reversibly and dose-dependently suppress outward K<sup>+</sup> channel currents in rat RGCs, which may be one of the possible mechanisms underlying Erigeron breviscapus prevents vision loss and RGC damage caused by glaucoma.展开更多
基金Supported by National Major Science-Technology Project of Science and Technology Ministry-Major New Medicine Innovation (No.2009ZX09103-369)Key Project of Chinese Ministry of Education2014 Sichuan Province Academic and Technology Leaders Training Funds
文摘AIMTo investigate the effect of DSX, an active component extracted from Erigeron breviscapus, on the voltage-gated outward K<sup>+</sup> channel currents in rat retinal ganglion cells (RGCs) by using electrophysiological method, and to explore the possible mechanisms of DSX on optic nerve protection.METHODSOutward K<sup>+</sup> currents were recorded by using whole-cell patch-clamp techniques on acutely isolated rat RGCs. Outward K<sup>+</sup> currents were induced by a series of depolarizing voltage pulses from a holding potential of -70 mV to +20 mV in an increment of 10 mV.RESULTSExtracellular application of DSX voltage-dependently suppressed both the steady-state and peak current amplitudes of outward K<sup>+</sup> currents in rat RGCs. Furthermore, DSX reversibly and dose-dependently inhibited the amplitudes of outward K<sup>+</sup> currents of the cells. At +20 mV membrane potential DSX at the concentrations of 0.02 g/L and 0.05 g/L showed no significant effects on the currents. In contrast, DSX at higher concentrations (0.1 g/L, 0.2 g/L and 0.5 g/L) significantly suppressed the current amplitudes.CONCLUSIONThese results suggest that DSX reversibly and dose-dependently suppress outward K<sup>+</sup> channel currents in rat RGCs, which may be one of the possible mechanisms underlying Erigeron breviscapus prevents vision loss and RGC damage caused by glaucoma.
