Shuo Yin1, Zhong-Feng Wang2, Jun-Guo Duan1, Lu Ji1, Xue-Jing Lu1. 1. Key Laboratory for Visual Function and Ophthalmopathy, Chengdu University of Traditional Chinese Medicine, Chengdu 610032, Sichuan Province, China. 2. Institutes of Brain Science, Fudan University, Shanghai 200032, China.
Abstract
AIM: To investigate the effect of DSX, an active component extracted from Erigeron breviscapus, on the voltage-gated outward K(+) channel currents in rat retinal ganglion cells (RGCs) by using electrophysiological method, and to explore the possible mechanisms of DSX on optic nerve protection. METHODS: Outward K(+) currents were recorded by using whole-cell patch-clamp techniques on acutely isolated rat RGCs. Outward K(+) 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. RESULTS: Extracellular application of DSX voltage-dependently suppressed both the steady-state and peak current amplitudes of outward K(+) currents in rat RGCs. Furthermore, DSX reversibly and dose-dependently inhibited the amplitudes of outward K(+) 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. CONCLUSION: These results suggest that DSX reversibly and dose-dependently suppress outward K(+) 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.
AIM: To investigate the effect of DSX, an active component extracted from Erigeron breviscapus, on the voltage-gated outward K(+) channel currents in rat retinal ganglion cells (RGCs) by using electrophysiological method, and to explore the possible mechanisms of DSX on optic nerve protection. METHODS: Outward K(+) currents were recorded by using whole-cell patch-clamp techniques on acutely isolated rat RGCs. Outward K(+) 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. RESULTS: Extracellular application of DSX voltage-dependently suppressed both the steady-state and peak current amplitudes of outward K(+) currents in rat RGCs. Furthermore, DSX reversibly and dose-dependently inhibited the amplitudes of outward K(+) 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. CONCLUSION: These results suggest that DSX reversibly and dose-dependently suppress outward K(+) 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.