• Journal of Ginseng Research
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• 제22권3호
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• pp.155-160
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• 1998

This stuffy was carried to establish a new efficient method for the preparation of edible crude ginseng saponin. The conventional butanol extraction and resin adsorption methods were compared for the contents of total crude ginseng saponin and major ginsenosides. Seventy- percent methanol extract was applied to Diaion HP-20 column and the resin was washed with Hn and eluted with absolute methanol. The methanol elute was dried in vivo and analyzed for its ginsenosides. Use of ethanol instead of methanol to make edible crude ginseng saponin gave a similar result. Butanol extraction was performed by the conventional method. The final aqueous layer from butanol extraction was passed through Diaion HP-20 column followed by elution with methanol and Diaion HP-20 passed fraction was extracted with butanol to recover remaining components, respectively, in order to determine saponin loss. TLC and HPLC qualitatively and quantitatively monitored Ginsenosides, respectively. Loss of ginsenosides was higher in butanol extraction method than in Diction HP-20 adsorption method. In addition, saponin fractions prepared by Diction HP-20 adsorption method showed higher content of each ginsenoside, showing 8.2% higher purity than that of butanol extracted fraction. From these results, we propose the resin adsorption method as a new efficient measure for the preparation of crude ginseng saponin, which is edible by using spirit instead of methanol.

• Journal of Ginseng Research
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• 제19권3호
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• pp.219-224
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• 1995

The modulatory effects of total ginseng saponin (TGS) on the 1, 6, and opioid receptor binding in morphine tolerance and dependence were examined in this study. The specific [$^{3}H$]DAGO ([D-$Ala^2$, N-$Mephe^4$, $Glyco^4$] enkephalin) binding was significantly increased in chronic morphine (10 mg/kg, i.p.) treated mouse striatum. The specific [$^{3}H$]DPDPE ([D-$Pen^2$, D-$Pen^5$] enkephalin) binding was ignificantly increased following morphine treatment in the mouse striatum and cortex. Also, an apparent decrease in the affinity of [$^{3}H$]DPN (diprenorphine) was observed after chronic morphine treatment in mouse striatum and cortex. 7GS produced a sleight increase of specific [$^{3}H$]DAGO, [$^{3}H$]DPDPE binding and a significant increase of specific [$^{3}H$]DPN binding in the mouse brain striatum. In cortex, TGS produced an inhibition of specific [$^{3}H$]DAGO and [$^{3}H$]DPDPE binding and increase of the specific [$^{3}H$]DPN binding. The prolonged administration of TGS (25, 50, 100, and 150 mg/kg, i.p., 3 wks) produced an inhibition of increased [$^{3}H$]DAGO specific binding following morphine without significant changes in the agonist binding to and receptors in mouse striatum and cortex. These contracted alterations in $\mu$, $\gamma$ and $\kappa$ opiate receptor binding were dependent in TGS dogs and brain sites.

• Archives of Pharmacal Research
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• 제12권3호
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• pp.166-175
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• 1989

In the previous observations, it was reported that both total ginseng saponin and panaxadiol revealed the marked secretory effect of catecholamines (CA) from the rabbit adrenal gland and that CA secretion induced by them is due to dual mechanisms, cholinergic action and the direct action. In the present study, an attempt to investigate the effect of panaxatriol-type saponin (PT), which is known as an active component of Korean ginseng, on the secretion of CA from the rabbit adrenal gland was made. PT(200 $\mu$g) administered into adrenal vein evoked significantly secretion of CA from the isolated perfused rabbit adrenal gland. Secretory effect of CA produced by PT was attenuated clearly by treatment with chlorisondamine or adenosine, but was markedly increased by physostigmine. Perfusion of Krebs solution containing PT (200 $\mu$g) for 30 min potentiated greatly secretion of CA induced by acetylcholine. PT-induced CA secretion was weakened considerably by ouabain treatement or perfusion of calcium-free Krebs solution. These experimental data demonstrate that PT releases CA from the isolated perfused rabbit adrenal gland by a calcium-dependentd exocytotic mechanism. It seems that the secretory effect of PT is caused through the release of acetylcholine form cholinergic terminals present in the adrenal gland and a direct action on the chromaffin cell itself.