Kim H S, Lee J H, Goo Y S, Nah S Y
Department of Pharmacology, College of Pharmacy, Chungbuk National University, Cheongju, Korea.
Brain Res Bull. 1998 Jun;46(3):245-51. doi: 10.1016/s0361-9230(98)00014-8.
We investigated the effects of ginseng total saponins (GTS) and five ginsenosides on voltage-dependent Ca2+ channels and membrane capacitance using rat adrenal chromaffin cells. In this study, cells were voltage-clamped in a whole-cell recording mode and a perforated patch-clamp technique was used. The inward Ca2+ currents (I(Ca)) was elicited by depolarization and the change in cell membrane capacitance (deltaCm) was monitored. The application of GTS (100 microg/ml) induced rapid and reversible inhibition of the Ca2+ current by 38.8 +/- 3.6% (n = 16). To identify the particular single component that seems to be responsible for Ca2+ current inhibition, the effects of five ginsenosides (ginsenoside Rb1, Rc, Re, Rf, and Rg1) on the Ca2+ current were examined. The inhibitions to the Ca2+ current by Rb1, Rc, Re, Rf, and Rg1 were 15.3 +/- 2.2% (n = 5); 36.9 +/- 2.4% (n = 7); 28.1 +/- 1.9% (n = 12); 19.0 +/- 2.5% (n = 10); and 16.3 +/- 1.6% (n = 15), respectively. The order of inhibitory potency (100 microM) was Rc > Re > Rf > Rg1 > Rb1. A software based phase detector technique was used to monitor membrane capacitance change (deltaCm). The application of GTS (100 microg/ml) induced inhibitory effects on deltaCm by 60.8 +/- 9.7% (n = 10). The inhibitions of membrane capacitance by Rb1, Rc, Re, Rf, and Rg1 were 35.3 +/- 5.5% (n = 7); 41.8 +/- 7.0% (n = 8); 40.5 +/- 5.9% (n = 9); 51.2 +/- 7.6% (n = 9); and 35.9 +/- 5.1% (n = 10), respectively. The inhibitory potencies of the ginsenosides on deltaCm were Rf > Rc > Re > Rg1 > Rb1. Therefore, we found that GTS and ginsenosides exerted inhibitory effects on both Ca2+ currents and deltaCm in rat adrenal chromaffin cells. These results suggest that ginseng saponins regulate catecholamine secretion from adrenal chromaffin cells and this regulation could be the cellular basis of antistress effects induced by ginseng.
我们使用大鼠肾上腺嗜铬细胞研究了人参总皂苷(GTS)和五种人参皂苷对电压依赖性Ca2+通道和膜电容的影响。在本研究中,细胞采用全细胞记录模式进行电压钳制,并使用穿孔膜片钳技术。通过去极化诱发内向Ca2+电流(I(Ca)),并监测细胞膜电容的变化(deltaCm)。应用GTS(100微克/毫升)可使Ca2+电流迅速且可逆地抑制38.8±3.6%(n = 16)。为了确定似乎对Ca2+电流抑制起作用的特定单一成分,研究了五种人参皂苷(人参皂苷Rb1、Rc、Re、Rf和Rg1)对Ca2+电流的影响。Rb1、Rc、Re、Rf和Rg1对Ca2+电流的抑制率分别为15.3±2.2%(n = 5);36.9±2.4%(n = 7);28.1±1.9%(n = 12);19.0±2.5%(n = 10);和16.3±1.6%(n = 15)。抑制效力顺序(100微摩尔)为Rc > Re > Rf > Rg1 > Rb1。使用基于软件的鉴相器技术监测膜电容变化(deltaCm)。应用GTS(100微克/毫升)对deltaCm产生60.8±9.7%的抑制作用(n = 10)。Rb1、Rc、Re、Rf和Rg1对膜电容的抑制率分别为35.3±5.5%(n = 7);41.8±?7.0%(n = 8);40.5±5.9%(n = 9);51.2±7.6%(n = 9);和35.9±5.1%(n = 10)。人参皂苷对deltaCm的抑制效力顺序为Rf > Rc > Re > Rg1 > Rb1。因此,我们发现GTS和人参皂苷对大鼠肾上腺嗜铬细胞的Ca2+电流和deltaCm均有抑制作用。这些结果表明,人参皂苷调节肾上腺嗜铬细胞中儿茶酚胺的分泌,这种调节可能是人参与抗应激作用的细胞基础。 (注:原文中“41.8±?7.0%”疑似有误,已按原样翻译)