• Proceedings of the Ginseng society Conference
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• 2005.11a
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• pp.32-40
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• 2005

The last two decades have shown a marked expansion in publications of diverse effects of Panax ginseng. Ginsenosides, as active ingredients of Panax ginseng, are saponins found in only ginseng. Recently, a line of evidences shows that ginsenosides regulate various types of ion channel activity such as Ca$^{2+}$, K$^+$, Na$^+$, Cl$^-$, or ligand gated ion channels (i.e. 5-HT$_3$, nicotinic acetylcholine, or NMDA receptor) in neuronal, non-neuronal cells, and heterologously expressed cells. Ginsenosides inhibit voltage-dependent Ca$^{2+}$, K$^+$, and Na$^+$ channels, whereas ginsenosides activate Ca$^{2+}$-activated Cl$^-$ and Ca$^{2+}$-activated K$^+$ channels. Ginsenosides also inhibit excitatory ligand-gated ion channels such as 5-HT$_3$. nicotinic acetylcholine, and NMDA receptors. This presentation will introduce recent findings on the ginsenoside-induced differential regulations of ion channel activities as a ligand as other drugs do.

• 한국가시화정보학회:학술대회논문집
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• 2005.12a
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• pp.80-84
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• 2005

Many important properties in colloidal systems are usually determined by surface charge ($\zeta$-potential) of the contacted solid surface. In this study, $\zeta$-potential of glass $\mu$-channel was evaluated from the electro-osmotic velocity distribution. The electro-osmotic velocity inside a glass $\mu$-channel was measured using a micro-PIV velocity field measurement technique. This evaluation method is more simple and easy to approach, compared with the traditional streaming potential technique. The $\zeta$-potential in the glass $\mu$-channel was measured for two different mole NaCl solutions. The effect of an anion surfactant, sodium dodecyl sulphate (SDS), on the electro-osmotic velocity and $\zeta$-potential in the glass surface was also studied. In the range of $0\∼6$mM, the surfactant SDS was added to NaCl solution in four different mole concentrations. As a result, the addition of SDS increases $\zeta$-potential in the surface of the glass $\mu$-channel. The measured $\zeta$-potential was found to vary from-260 to-70mV. When negatively charged particles were used, the flow direction was opposite compared with that of neutral particles. The $\zeta$-potential has a positive sign for the negative particles.

• Transactions of the Korean Society of Mechanical Engineers B
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• v.30 no.10 s.253
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• pp.935-941
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• 2006

Many important properties in colloidal systems are usually determined by surface charge $({\zeta}-potential)$ of the contacted solid surface. In this study, ${\zeta}-potential$ of glass ${\mu}-channel$ was evaluated from the electro-osmotic velocity distribution. The electro-osmotic velocity inside a glass f-channel was measured using a micro-PIV velocity field measurement technique. This evaluation method is more simple and easy to approach, compared with the traditional streaming potential technique. The ${\zeta}-potential$ in the glass ${\mu}-channel$ was measured fur two different mole NaCl solutions. The effect of an anion surfactant, sodium dodecyl sulphate (SDS), on the electro-osmotic velocity and f-potential in the glass surface was also studied. In the range of $0{\sim}6mM$, the surfactant SDS was added to NaCl solution in few different mole concentrations. As a result, the addition of SDS increases ${\zeta}-potential$ in the surface of the glass ${\mu}-channel$. The measured $\zeta-potential$ was found to vary from -260 to -70mV. When negatively charged particles were used, the flow direction was opposite compared with that of neutral particles. The ${\zeta}-potential$ has a positive sign for the negative particles.

• Molecules and Cells
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• v.19 no.1
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• pp.137-142
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• 2005

We showed recently that ginsenosides inhibit the activity of various types of ion channel. Here we have investigated the role of the carbohydrate component of ginsenoside $Rg_3$ in the inhibition of $Na^+$ channels. The channels were expressed in Xenopus oocytes by injecting cRNAs encoding rat brain Nav1.2 ${\alpha}$ and ${\beta}1$ subunits, and analyzed by the two-electrode voltage clamp technique. Treatment with $Rg_3$ reversibly inhibited the inward $Na^+$ peak current ($I_{Na}$) with an $IC_{50}$ of $32.2{\pm}4.5{\mu}M$, and the inhibition was voltage-dependent. To examine the role of the sugar moiety, we prepared a straight chain form of the second glucose and a conjugate of this glucose with 3-(4-hydroxyphenyl) propionic acid hydrazide (HPPH). Neither derivative inhibited $I_{Na}$. Treatment with the carbohydrate portion of ginsenoside $Rg_3$, sophorose [${\beta}-D-glucopyranosyl$ ($1{\rightarrow}2$)-${\beta}-glucopyranoside$], or the aglycone (protopanaxadiol), on their own or in combination had no effect on $I_{Na}$. These observations indicate that the carbohydrate portion of ginsenoside $Rg_3$ plays an important role in its effect on the $Na^+$ channel.

• Journal of Life Science
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• v.2 no.2
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• pp.97-107
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• 1992

Strichartz and Richie have suggested that the mechanism of sodium donductance block of local anesthetics involves their interaction with a specific binding site within the sodium channel. However, there is evidence that local anesthetics can interact electrostatically with membrane proteins as well as membrane lipids. Whether or not all actions of local anesthetics are mediated by common site remains unclear. Thus, it can not be ruled out that local anesthetics concurrently interact with neuronal membrane lipids since sodium channels were found to be tightly associated with membrane lipids through covalent or noncovalent bonds. In summary, it is strongly postulated that local anesthetics, in addition to their direct interaction with sodium channels, concurrently interact with membrane lipids, fluidize the membrane, and thus induce conformational changes of sodium channels, which are known to be tightly associated with membrane lipids.

• Journal of Ginseng Research
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• v.29 no.1
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• pp.19-26
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• 2005

The last two decades have shown a marked expansion in publications of diverse effects of Panax ginseng. Ginsenosides, as active ingredients of Panax ginseng, are saponins found in only ginseng. Recently, a line of evidences shows that ginsenosides regulate various types of ion channel activity such as $Ca^{2+},\;K^+,\;Na^+,\;Cl^-$, or ligand gated ion channels (i.e. $5-HT_3$, nicotinic acetylcholine, or NMDA receptor) in neuronal, non-neuronal cells, and heterologously expressed cells. Ginsenosides inhibit voltage-dependent $Ca^{2+},\;K^+,\;and\;Na^+$ channels, whereas ginsenosides activate $Ca^{2+}-activated\;Cl^-\;and\;Ca^{2+}-activated\;K^+$ channels. Ginsenosides also inhibit excitatory ligand-gated ion channels such as $5-HT_3$, nicotinic acetylcholine, and NMDA receptors. This review will introduce recent findings on the ginsenoside-induced differential regulations of ion channel activities and will further expand the possibilities how these ginsenoside-induced ion channel regulations are coupled to biological effects of Panax ginseng.

• Advances in Traditional Medicine
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• v.4 no.3
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• pp.157-161
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• 2004

We showed the effects of the traditional herbal medicine, Jukyeoondam-tang (JO-T, Zhu-ru-Wen-Dan-Tang in Chinese), on ventricular arrhythmia induced by aconitine. Electrophysiological experiments with conventional microelectrode techniques revealed that JO-T potently suppressed the aconitine-induced arrhythmias in ventricular strips of the rat. In the aconitine-induced arrhythmia model of the rat, pretreatment with JO-T $(100\;{\mu}g/ml)$ completely occluded the appearance of ventricular tachyarrhythmia (VT) or ventricular fibrillation (VF) induced by aconitine. Furthermore, the aconitine-induced ventricular arrhythmia was occluded by $Na^+$ channel blocker quinidine but was not occluded by $K^+$ channel blocker glibenclamide $(3\;{\mu}mol/L)\;and\;Ca^{2+}$ channel blocker nifedipine $(10\;{\mu}mol/L)$. We also confirmed the effect of JO-T in the ischemia-reperfusion (I/R)-induced arrhythmia model of the rat. JO-T did not affect the I/R-induced arrhythmias in rats. JO-T may alleviate the risk of ventricular arrhythmias following aconitine. These results suggest that JO-T is a potent antiarrhythmic drug having a$Na^+$ channel-blocking action.

• The Korean Journal of Physiology and Pharmacology
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• v.17 no.1
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• pp.57-64
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• 2013

Cells can resist and even recover from stress induced by acute hypoxia, whereas chronic hypoxia often leads to irreversible damage and eventually death. Although little is known about the response(s) to acute hypoxia in neuronal cells, alterations in ion channel activity could be preferential. This study aimed to elucidate which channel type is involved in the response to acute hypoxia in rat pheochromocytomal (PC12) cells as a neuronal cell model. Using perfusing solution saturated with 95% $N_2$ and 5% $CO_2$, induction of cell hypoxia was confirmed based on increased intracellular $Ca^{2+}$ with diminished oxygen content in the perfusate. During acute hypoxia, one channel type with a conductance of about 30 pS (2.5 pA at -80 mV) was activated within the first 2~3 min following onset of hypoxia and was long-lived for more than 300 ms with high open probability ($P_o$, up to 0.8). This channel was permeable to $Na^+$ ions, but not to $K^+$, $Ca^+$, and $Cl^-$ ions, and was sensitively blocked by amiloride (200 nM). These characteristics and behaviors were quite similar to those of epithelial sodium channel (ENaC). RT-PCR and Western blot analyses confirmed that ENaC channel was endogenously expressed in PC12 cells. Taken together, a 30-pS ENaC-like channel was activated in response to acute hypoxia in PC12 cells. This is the first evidence of an acute hypoxia-activated $Na^+$ channel that can contribute to depolarization of the cell.

• The Korean Journal of Physiology and Pharmacology
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• v.1 no.4
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• pp.367-376
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• 1997

The effect of an organic peroxide, t-butylhydroperoxide (t-BHP), on glutamate uptake was studied in synaptosomes prepared from cerebral cortex. t-BHP inhibited the $Na^+-dependent$ glutamate uptake with no change in the $Na^+-independent$ uptake. This effect of t-BHP was not altered by addition of $Ca^{2+}$ channel blockers (verapamil, diltiazem and nifedipine) or $PLA_2$ inhibitors (dibucaine, butacaine and quinacrine). However, the effect was prevented by iron chelators (deferoxamine and phenanthroline) and phenolic antioxidants (N,N'-diphenyl-phenylenediamine, butylated hydroxyanisole, and butylated hydroxytoluene). At low concentrations (＜1.0 mM), t-BHP inhibited glutamate uptake without altering lipid peroxidation. Moreover, a large increase in lipid peroxidation by $ascorbate/Fe^{2+}$ was not accompanied by an inhibition of glutamate uptake. The impairment of glutamate uptake by t-BHP was not intimately related to the change in $Na^+-K+-ATPase$ activity. These results suggest that inhibition of glutamate uptake by t-BHP is not totally mediated by peroxidation of membrane lipid, but is associated with direct interactions of glutamate transport proteins with t-BHP metabolites. The $Ca^{2+}$ influx through $Ca^{2+}$ channel or $PLA_2$ activation may not be involved in the t-BHP inhibition of glutamate transport.

• Journal of Photoscience
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• v.3 no.3
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• pp.133-136
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• 1996

Calcium modulates the activity of guanylate cyclase and plays a key role in dark and light adaptation in the visual system. We have measured the Ca$^{2+}$, K$^+$ and Na$^+$ concentration in dark and light adapted bullfrog's (Rana catesbeiana) vitreous humor by using the atomic absorption spectrophotometer. The calcium concentration of the light adapted bullfrog's vitreous humor was higher than that of the dark adapted bullfrog's vitreous humor. This means that ion activity between the photoreceptor and vitreous humor side is light dependent and we have found that a Ca$^{2+}$ channel and Na$^+$ - Ca$^{2+}$ exchanger exist in the vitreous humor.