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灯盏细辛提取物(DSX)调节大鼠视网膜神经节细胞的外向钾电流。

Extraction (DSX) from Erigeron breviscapus modulates outward potassium currents in rat retinal ganglion cells.

作者信息

Yin Shuo, Wang Zhong-Feng, Duan Jun-Guo, Ji Lu, Lu Xue-Jing

机构信息

Key Laboratory for Visual Function and Ophthalmopathy, Chengdu University of Traditional Chinese Medicine, Chengdu 610032, Sichuan Province, China.

Institutes of Brain Science, Fudan University, Shanghai 200032, China.

出版信息

Int J Ophthalmol. 2015 Dec 18;8(6):1101-6. doi: 10.3980/j.issn.2222-3959.2015.06.04. eCollection 2015.

DOI:10.3980/j.issn.2222-3959.2015.06.04
PMID:26682155
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4651871/
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.

摘要

目的

采用电生理方法研究灯盏花中提取的活性成分灯盏细辛素(DSX)对大鼠视网膜神经节细胞(RGCs)电压门控外向钾离子通道电流的影响,并探讨DSX对视神经保护的可能机制。

方法

采用全细胞膜片钳技术记录急性分离的大鼠RGCs的外向钾离子电流。通过从-70 mV的钳制电位以10 mV的增量到+20 mV的一系列去极化电压脉冲诱导外向钾离子电流。

结果

细胞外应用DSX电压依赖性地抑制大鼠RGCs外向钾离子电流的稳态和峰值电流幅度。此外,DSX可逆且剂量依赖性地抑制细胞外向钾离子电流的幅度。在膜电位为+20 mV时,0.02 g/L和0.05 g/L浓度的DSX对电流无显著影响。相比之下,较高浓度(0.1 g/L、0.2 g/L和0.5 g/L)的DSX显著抑制电流幅度。

结论

这些结果表明,DSX可逆且剂量依赖性地抑制大鼠RGCs外向钾离子通道电流,这可能是灯盏花预防青光眼导致的视力丧失和RGC损伤的可能机制之一。

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