Comparison of the pharmacological effects of Panax ginseng and Panax quinquefolium

Medical application of Panax ginseng was first found in "Shen-Nong Herbal Classic"around 200 AD Panax quinquefolium was first introduced in "Essential of Materia Medica" in 1694 in China. The most important bioactive components contained in P ginseng and P quinquefolium are ginseng saponins (GS). The contents of ginsenoside Rb1, Re, and Rd in P quinquefolium are higher than they are in P ginseng. In P ginseng, the contents of Rg1,Rb2, and Rc are higher than they are in P quinquefolium. P ginseng had a higher ratio of Rg1: Rb1, and which was lower in P quinquefolium. After steaming for several hours, the total GS will decrease. However, some ginsenosides (Rg2, 20R-Rg2, Rg3, Rh1 and Rh2) increase, while others (Rb1, Rb2, Rb3, Rc, Rd, Re, and Rg1) decrease. However, variation, especially in P quinquefolium, is high. P ginseng and P quinquefolium are general tonics and adaptogens. Rg1 and Rb1 enhance central nervous system (CNS) activities, but the effect of the latter is weaker. Thus, for the higher contents of Rg1, P ginseng is a stimulant, whereas the Rb1 contents of P quinquefolium are mainly calming to the CNS. Re, Rg1, panaxan A and B from P ginseng are good for diabetes. Re and Rg1 enhance angiogenesis, whereas Rb1, Rg3 and Rh2 inhibit it. Rh2, an antitumor agent, can be obtained from Rb1 by steaming. The content of Re in P quinquefolium are higher than in P ginseng by 3-4 times. The vasorelax, antioxidant, antihyperlipidemic, and angiogenic effects of Re are reported. Thus, for the CNS "hot," wound healing and hypoglycemic effects, P ginseng is better than P quinquefolium. For anticancer effects, P quinquefolium is better.     

Studies on antinephritic effects of plant components in rats (2): Effects of ginsenosides on original-type anti-GBM nephritis in rats and its mechanisms

To clarify the antinephritic effects of ginsenosides, we investigated the effects of crude ginsenoside and ginsenosides Rg1 and Rb1 on original-type anti-GBM nephritis in rats. Crude ginsenoside at 1.0 mg and 5.0 mg/kg, i.p., and ginsenoside Rg1 at 1.0 mg/kg, i.p., prevented urinary protein excretion and elevation of serum cholesterol content, as well as histopathological changes such as hypercellularity and adhesion. On the other hand, ginsenoside Rb1 only inhibited the histopathological parameters. In order to clarify the antinephritic mechanisms of ginsenosides on this model, we investigated the effect of ginsenosides on platelet aggregation and renal blood flow. Crude ginsenoside markedly enhanced the renal blood flow. Ginsenoside Rg1 inhibited the platelet aggregation in vivo and enhanced the renal blood flow on the 1st day. These results suggest that crude ginsenoside and Rg1 exert their antinephritic action via increased renal blood flow.     

Ginsenoside Rg3 mediates endothelium-dependent relaxation in response to ginsenosides in rat aorta: role of K+ channels

The aim of the present study was to characterize the endothelium-dependent relaxation elicited by ginsenosides, a mixture of saponin extracted from Panax ginseng, in isolated rat aorta. Relaxations elicited by ginsenosides were mimicked by ginsenoside Rg1 and ginsenoside Rg1, two major ginsenosides of the protopanaxatriol group. Ginsenoside Rg3 was about 100-fold more potent than ginsenoside Rg1. The endothelium-dependent relaxation in response to ginsenoside Rg3 was associated with the formation of cycle GMP. These effects were abolished by N(G)-nitro-L-arginine and methylene blue. Relaxations in response to ginsenoside Rg3 were unaffected by atropine, diphenhydramine, [D-Pro2, D-Trp7,9]substance P, propranolol, nifedipine, verapamil and glibenclamide but were markedly reduced by tetraethylammonium. Tetraethylammonium modestly reduced the relaxation induced by sodium nitroprusside. These findings indicate that ginsenoside Rg3 is a major mediator of the endothelium-dependent nitric oxide-mediated relaxation in response to ginsenosides in isolated rat aorta, possibly via activation of tetraethylammonium-sensitive K+ channels.     

Enzymatic preparation of ginsenosides Rg2, Rh1, and F1 from protopanaxatriol-type ginseng saponin mixture

During investigations on the hydrolysis of a protopanaxatriol-type saponin mixture by various glycoside hydrolases, it was found that two minor saponins, ginsenosides Rg 2 and Rh 1, were formed in high yields by crude beta-galactosidase from Aspergillus oryzae and crude lactase from Penicillium sp., respectively. Moreover, a crude preparation of naringinase from Penicillium decumbens readily hydrolyzed a protopanaxatriol-type saponin mixture to give an intestinal bacterial metabolite, ginsenoside F 1 as the main product. A crude preparation of hesperidinase from Penicillium sp. selectively hydrolyzed ginsenoside Re into ginsenoside Rg 1. This is the first report on the enzymatic preparation of minor saponins, ginsenosides Rg 2 and Rh 1, and of an intestinal bacterial metabolite, ginsenoside F 1, with a high efficiency from a protopanaxatriol-type saponin mixture.     

高效液相色谱法用于西洋参与白参的分析和鉴别

采用高效液相色谱法测定了１０个不同地区栽培的西洋参与白参中人参皂苷 Ｒｂ１的含量,并利用相对保留时间和相对含量对两者进行定性鉴别     

西洋参药材的等级标准及质量评价研究

目的建立西洋参药材的等级标准,并对不同等级药材的质量进行评价。方法以24批西洋参药材为样本,采用Pearson相关性分析方法对定性分析指标(主根长度、主根直径和单根药材质量)与内在成分指标(醇溶性浸出物及人参皂苷Rg1、人参皂苷Re、人参皂苷Rb1、人参皂苷Rc、人参皂苷Rb2、人参皂苷Rd、拟人参皂苷F11的含量)间的相关性进行分析,结合化学计量学方法筛选出西洋参等级划分的参考指标,并制定等级划分标准。建立24批西洋参药材的高效液相色谱-蒸发光散射检测器(HPLC-ELSD)指纹图谱并进行相似度评价,通过与对照品比对进行色谱峰的指认,然后结合聚类分析对不同等级西洋参药材进行质量评价。结果经筛选,确定主根直径、单根药材质量和人参皂苷Rd含量为西洋参药材等级划分的参考指标。根据上述3个指标,将西洋参药材分为特等、一等和二等3个等级。根据K-均值聚类的中心值,算出特等药材的总得分>135.40,一等药材的总得分为61.82~135.40,二等药材的总得分<61.82。从24批西洋参药材的HPLC-ELSD指纹图谱中,共确定了25个共有峰,并指认了其中7个特征峰;特等、一等、二等西洋参药材的色谱图与对照指纹图谱的相似度分别为0.980~0.989、0.962~0.968、0.940~0.949。聚类分析结果显示,不同等级西洋参药材可被明显区分开。结论本研究建立了西洋参药材的等级标准和HPLC-ELSD指纹图谱,可应用于西洋参药材的专属鉴别,并为其质量控制及等级划分提供参考。     

Transformation of ginseng saponins to ginsenoside rh<Subscript>2</Subscript> by acids and human intestinal bacteria and biological activities of their transformants

When ginseng water extract was incubated at 60 degrees C in acidic conditions, its protopanaxadiol ginsenosides were transformed to ginsenoside Rg3 and delta20-ginsenoside Rg3. However, protopanaxadiol glycoside ginsenosides Rb1, Rb2 and Rc isolated from ginseng were mostly not transformed to ginsenoside Rg3 by the incubation in neutral condition. The transformation of these ginsenosides to ginsenoside Rg3 and delta20-ginsenoside Rg3 was increased by increasing incubation temperature and time in acidic condition: the optimal incubation time and temperature for this transformation was 5 h and 60 degrees C resepectively. The transformed ginsenoside Rg3 and delta20-ginsenoside Rg3 were metabolized to ginsenoside Rh2 and delta20-ginsenoside Rh2, respectively, by human fecal microflora. Among the bacteria isolated from human fecal microflora, Bacteroides sp., Bifidobacterium sp. and Fusobacterium sp. potently transformed ginsenoside Rg3 to ginsenoside Rh2. Acid-treated ginseng (AG) extract, fermented AG extract, ginsenoside Rh2 and protopanaxadiol showed potent cytotoxicity against tumor cell lines. AG extract, fermented AG extract and protopanaxadiol potently inhibited the growth of Helicobacter pylori.     

Effects of ginsenosides,active components of ginseng,on nicotinic acetylcholine receptors expressed in Xenopus oocytes

We investigated the effects of ginsenosides, the active ingredient of ginseng, on neuronal or muscle-type nicotinic acetylcholine receptor channel activity expressed in Xenopus oocytes after injection of cRNA encoding bovine neuronal alpha3beta4, alpha7 or human muscle alphabetadeltavarepsilon subunits. Treatment with acetylcholine elicited an inward peak current (I(ACh)) in oocytes expressing nicotinic acetylcholine receptor subtypes. Cotreatment with ginsenoside Rg2 and acetylcholine inhibited I(ACh) in oocytes expressing with alpha3beta4 or alphabetadeltavarepsilon but not in oocytes expressing alpha7 nicotinic acetylcholine receptors. The inhibition of I(ACh) by ginsenoside Rg2 was reversible and dose-dependent. The half-inhibitory concentrations (IC50) of ginsenoside Rg2 were 60.2+/-14.1 and 15.7+/-3.5 microM in oocytes expressing alpha3beta4 and alphabetadeltavarepsilon nicotinic acetylcholine receptors, respectively. The inhibition of I(ACh) by ginsenoside Rg2 was voltage-independent and noncompetitive. Other ginsenosides besides ginsenoside Rg2 also inhibited I(ACh) in oocytes expressing alpha3beta4 or alphabetadeltavarepsilon nicotinic acetylcholine receptors. The order of potency for the inhibition of I(ACh) was ginsenoside Rg2>Rf>Re>Rg1>Rc>Rb2>Rb1 in oocytes expressing alpha3beta4 nicotinic acetylcholine receptors and was ginsenoside Rg2>Rf>Rg1>Re>Rb1>Rc>Rb2 in oocytes expressing alphabetadeltavarepsilon nicotinic acetylcholine receptors. These results indicate that ginsenosides might regulate nicotinic acetylcholine receptors in a differential manner and this regulation might be one of the pharmacological actions of Panax ginseng.     

Metabolism of ginsenoside Re by human intestinal microflora and its estrogenic effect

To understand the relationship between the metabolism and biological activity of ginsenoside Re, a main protopanaxatriol saponin in Panax ginseng C. A. MEYER, its metabolic pathway and estrogenic effect by human intestinal microflora were investigated. All human fecal specimens metabolized ginsenoside Re, mainly to ginsenoside Rh1 and ginsenoside F1, via ginsenoside Rg1, with protopanaxadiol as a minor component. Almost all isolated ginsenoside Re-metabolizing intestinal bacteria (GHIB) also metabolized ginsenoside Re, mainly to ginsenosides Rh1 and F1, via ginsenoside Rg1. Alpha-Rhamnosidase and beta-glucosidase, partially purified from the most potent GHIB, Bacteroides JY-6, hydrolyzed ginsenoside Re and ginsenoside Rg1, respectively; however, they did not hydrolyze ginsenosides Rh1 and F1. These findings suggest that the ginsenosides Rh1 and/or F1 may not be suitable substrates of intestinal bacteria, particularly Bacteroides JY-6. The estrogenic effects of ginsenoside Re and its main metabolites, ginsenosides Rg1 and Rh1, were also investigated. Ginsenoside Rh1 showed the greatest estrogenic effect in human breast carcinoma MCF-7 cells. Based on these findings, the estrogenic effect of ginsenoside Re may be expressed by intestinal microflora.     

The antistress effect of ginseng total saponin and ginsenoside Rg3 and Rb1 evaluated by brain polyamine level under immobilization stress.

The present study aims to demonstrate the ability of ginseng total saponin (GTS), ginsenosides Rg3 and Rb1 to reduce brain polyamine levels in immobilization-stressed gerbil mice. A previous study reported that ginsenosides had an anti-stress property. So, we tested the anti-stress effect of ginseng by investigating the brain level of polyamine, a well-known stress stimuli marker. We determined the brain polyamine levels under 30-min immobilization stress in pretreating GTS (100 mgkg(-1), oral), ginsenosides Rg3 and Rb1 (10 mgkg(-1), oral, respectively). Then, we compared polyamine levels between the non-stressed mouse and the stressed mouse which had taken saline orally to check the placebo effect. Putrescine (PUT) levels were significantly increased (P < 0.01) in the stressed condition, but it was reduced in pretreatment of GTS, ginsenosides Rg3 (P < 0.01, respectively) and Rb1 (P < 0.001) under 30-min immobilization stressed-mouse. However, other polyamine levels did not change regardless of stressed condition or GTS-, ginsenosides Rg3- and Rb1-treated stressed condition. These results mean that only PUT could be a marker for stress and GTS, ginsenosides Rg3 and Rb1 administration lead to an anti-stress effect. Thus, our studies indicate that GTS, ginsenosides Rg3 and Rb1 may play a neuroprotective role in the immobilization-stressed brain.     

Inhibitory effect of ginsenoside Rg5 and its metabolite ginsenoside Rh3 in an oxazolone-induced mouse chronic dermatitis model

The effect of a main constituent ginsenoside Rg5 isolated from red ginseng and its metabolite ginsenoside Rh3 in a chronic dermatitis model was investigated. Ginsenosides Rg5 and Rh3 suppressed swelling of oxazolone-induced mouse ear contact dermatitis. These ginsenosides also reduced mRNA expressions of cyclooxygenase-2, interleukin (IL)-1beta, tumor necrosis factor (TNF)-alpha and interferon (IFN)-gamma. The inhibition of ginsenoside Rh3 was more potent than that of ginsenoside Rg5. These findings suggest that ginsenoside Rh3 metabolized from ginsenoside Rg5 may improve chronic dermatitis or psoriasis by the regulation of IL-1beta and TNF-alpha produced by macrophage cells and of IFN-gamma produced by Th cells.     

Neurotrophic and neuroprotective actions of ginsenosides Rb(1) and Rg(1)

The ginsenosides have many pharmacological actions, including various actions on the nervous system. Our previous studies have demonstrated that two ginsenosides, Rb(1) and Rg(1) improve performance in a passive avoidance-learning paradigm and enhance cholinergic metabolism. The present study was designed to examine the cellular neurotrophic and neuroprotective actions of two pure ginsenosides in two model systems. PC12 cells were grown in the absence or presence of nerve growth factor (NGF) as a positive control, and different concentrations of Rb(1) or Rg(1). To assess neurotrophic properties, neurite outgrowth was quantified for representative fields of cells. After 8 days in culture, both ginsenosides enhanced neurite outgrowth in the presence of a sub-optimal dose of (2 ng/ml) NGF, but did not significantly stimulate neurite outgrowth in the absence of NGF. However, after 18 days in culture, both ginsenosides increased neurite outgrowth in the absence of NGF. SN-K-SH cells were grown in the absence or presence of MPTP or beta-amyloid to assess neuroprotection. Rb(1) and Rg(1) both reversed MPTP-induced cell death. beta-Amyloid-induced cell death was not reversed by either ginsenoside, but Rg(1) produced a modest enhancement of cell death in this model. These results suggest that these two ginsenosides have neurotrophic and selective neuroprotective actions that may contribute to the purported enhancement of cognitive function.     

Inhibitory effects of Korean red ginseng and its genuine constituents ginsenosides Rg3, Rf, and Rh2 in mouse passive cutaneous anaphylaxis reaction and contact dermatitis models

The inhibitory effects of the Korean red ginseng (steamed root of Panax ginseng C.A. MEYER, family Araliaceae) saponin fraction (KRGS) and its constituents ginsenosides Rg3, Rf, and Rh2 in mouse passive cutaneous anaphylaxis (PCA) and contact dermatitis models were measured. Orally administered KRGS and its genuine ginsenosides potently inhibited the PCA reaction induced by IgE. However, when these ginsenosides were intraperitoneally administered, ginsenoside Rh2 showed the most potent inhibition. The ginsenoside Rh2 also the most potently inhibited the beta-hexosaminidase release from RBL-2H3 cells induced by IgE with antigen. KRGS administered topically at a dose of 0.1% suppressed ear swelling in an oxazolone-induced mouse contact dermatitis model by 38.8%. Its constituents ginsenosides Rg3, Rf, and Rh2 at a concentration of 0.05% also potently suppressed mouse ear swelling by 47.5%, 34.8%, and 49.9% at 16 d, respectively. These ginsenosides also significantly reduced mRNA expression levels of cyclooxygenase (COX)-2, interleukin (IL)-1beta, tumor necrosis factor-alpha and interferon-gamma induced by oxazolone applied to mouse ears. However, the ginsenosides, except for ginsenoside Rh2, almost did not notably reduce IL-4 levels. The ginsenoside Rh2 also potently inhibited COX-2 and inducible NO synthetase protein expression in liphopolysaccharide-stimulated RAW264.7 cells. Based on these findings, KRGS and its ginsenosides are suggested to improve atopic and contact dermatitis by regulating expression of cytokines.     

Ginsenoside Rh2 reduces ischemic brain injury in rats

Ginseng was incubated under mildly acidic conditions and its inhibitory effect on a rat ischemia-reperfusion model was investigated. When ginseng was treated with 0.1% hydrochloric acid at 60 degrees C, its protopanaxadiol saponins were transformed to diasteromeric ginsenoside Rg3 and Delta20-ginsenoside Rg3. When the transformed ginseng extract, of which the main component was ginsenosides Rg3, was treated with human intestinal microflora, the main metabolite was ginsenoside Rh2. Orally administered acid-treated ginseng (AG) extract and ginsenoside Rh2 potently protect ischemia-reperfusion brain injury. The ginsenoside Rh2 also inhibited prostaglandin-E2 synthesis in lipopolysaccharide-stimulated RAW264.7 cells, but showed no in vitro antioxidant activity. These results suggest that AG and ginsenoside Rh2 can improve ischemic brain injury.     

Effects of ginsenosides on GABAA receptor channels expressed in xenopus oocytes

Ginsenosides, major active ingredients of Panax ginseng, are known to regulate excitatory ligand-gated ion channel activity such as nicotinic acetylcholine and NMDA receptor channel activity. However, it is not known whether ginsenosides affect inhibitory ligand-gated ion channel activity. We investigated the effect of ginsenosides on human recombinant GABA(A) receptor (alpha1beta1gamma2S) channel activity expressed in Xenopus oocytes using a two-electrode voltage-clamp technique. Among the eight individual ginsenosides examined, namely, Rb1, Rb2, Rc, Rd, Re, Rf, Rg1 and Rg2, we found that Rc most potently enhanced the GABA-induced inward peak current (I(GABA)). Ginsenoside Rc alone induced an inward membrane current in certain batches of oocytes expressing the GABA(A) receptor. The effect of ginsenoside Rc on I(GABA) was both dose-dependent and reversible. The half-stimulatory concentration (EC50) of ginsenoside Rc was 53.2 +/- 12.3 microM. Both bicuculline, a GABA(A) receptor antagonist, and picrotoxin, a GABA(A) channel blocker, blocked the stimulatory effect of ginsenoside Rc on I(GABA). Niflumic acid (NFA) and 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS), both Cl- channel blockers, attenuated the effect of ginsenoside Rc on I(GABA). This study suggests that ginsenosides regulated GABA(A) receptor expressed in Xenopus oocytes and implies that this regulation might be one of the pharmacological actions of Panax ginseng.     

Self-micelle formation and the incorporation of lipid in the formulation affect the intestinal absorption of Panax notoginseng

The purpose of this research is to evaluate the effect of self-micelle formation and incorporation of lipid in the formulation on absorption of ginsenosides Rg1 and Rb1 from intestinal tract in rats. Ginsenosides Rg1 and Rb1 were extracted from Panax notoginseng saponins (PNS). The critical micellar concentration (CMC) of PNS in deionzied water was determined to be 0.339 mg/ml. At normal physiological ionic strengths, PNS was salted out from the solution above the CMC. The particle size of the micelle grows as PNS concentration increases. By in situ injection to a closed loop of the rat jejunum, AUC0-6h obtained after administration of low concentration solution (12 mg/ml) was 3.61 times for ginsenoside Rg1 and 3.84-folds for ginsenoside Rb1 compared with high concentration solution (120 mg/ml). The release rate of ginsenosides in aqueous medium was too slow to complete in 24h, especially for Rb1. The data suggested that the self-micelle formation tendency in ginsenosides might prevent them from permeation or absorption through the cell membrane of gastrointestinal (GI) tract. To inhibit the formation of micelles, lipid was incorporated in the PNS formulation. The intraduodenal bioavailability in rats showed that the bioavailability was enhanced remarkably relative to the aqueous solution. AUC 0-infinity of ginsenoside Rg1 and Rb1 in the lipid-based formulation were 207.52+/-53.95 and 1961.72+/-686.60 microg ml(-1) h, compared with 7.87+/-2.85 and 148.58+/-36.73 microg ml(-1) h, respectively from its aqueous solution. These findings suggested a new strategy to increase the absorption of amphiphilic saponins.     

The ginsenoside Rg3 evokes endothelium-independent relaxation in rat aortic rings: role of K+ channels

The purpose of the present study was to characterize the mechanism underlying the direct relaxing activity of ginsenosides on vascular smooth muscle. The total ginsenoside mixture, ginsenosides from either the protopanaxadiol group or the protopanaxatriol group, and the ginsenoside Rg3 from the protopanaxatriol group caused a concentration-dependent relaxation of rat aortic rings without endothelium contracted with 25 x 10(-3) M KCl but affected only minimally those contracted with 60 x 10(-3) M KCl. Ginsenoside Rg3 was the most potent relaxing agonist. Relaxations elicited by ginsenoside Rg3 were markedly reduced by tetraethylammonium, a blocker of non-selective K+ channels, but not by glibenclamide, a blocker of ATP-sensitive K+ channels. Ginsenoside Rg3 significantly inhibited Ca2+-induced concentration-contraction curves and the 45Ca2+ influx in aortic rings incubated with 25 x 10(-3) M KCl whereas these responses were not affected in rings incubated with 60 x 10(-3) M KCl. Ginsenoside Rg3 caused a time- and concentration-dependent efflux of 86Rb from aortic rings that was inhibited by tetraethylammonium but not by glibenclamide. These findings indicate that ginsenoside Rg3 is a potent inhibitor of vascular smooth muscle tone and that this effect seems to be due to an inhibition of Ca2+ influx and stimulation of K+ efflux, possibly via activation of tetraethylammonium-sensitive K+ channels.     

Induction of apoptosis by ginsenoside Rk1 in SK-MEL-2-human melanoma

Ginsenosides are active compounds isolated from Panax ginseng Meyer. Among these ginsenosides, less polar ginsenosides such as ginsenoside Rg3 and ginsenoside Rh2 have been demonstrated to have tumor inhibitory effects because of their cytotoxicity. In this study, we evaluated the apoptotic effects of ginsenoside Rk1 in SK-MEL-2 human melanoma. Ginsenoside Rk1 isolated from red ginseng is one of the novel ginsenosides that shows strong cytotoxicity compared to ginsenoside Rg3 in dose- and time-dependent manners. The results of DNA fragmentation, 4′,6-diamidino-2-phenylindole staining, and flow cytometric analysis are corroborated that ginsenoside Rk1 induced apoptosis in SK-MEL-2 cells. Western blot analysis revealed up-regulation of Fas, FasL, and Bax protein expression and down-regulation of procaspase-8, procaspase-3, mutant p53 and Bcl-2 protein expression. These findings suggest that ginsenoside Rk1 might be a promising compound to induce apoptosis through both extrinsic and intrinsic pathways in SK-MEL-2 cells.     

Medicinal history and ginsenosides composition of Panax ginseng rhizome, "Rozu"

Ginseng is prepared from Panax ginseng C.A. Meyer root. The root of wild P. ginseng has long tortuous rhizome called traditionally "Rozu" in Japanese. In the present historical studies on ginseng, it has been proven that ginseng has sometimes been used after removing "Rozu" due to its emetic effects. However, ginseng with "Rozu" is prescribed in almost all the present Kampo formulations used clinically in China and Japan. Possible reasons for this are (1) some formulations including "Rozu" have been used for vomiting resulting from the retention of fluid in the intestine and stomach, "tan-in" in Japanese, and (2) the present cultivated ginseng has shorter "Rozu" than wild ginseng. Furthermore, it is proved that "Rozu", rich in ginsenoside Ro with oleanane-type aglycone, is distinguished from ginseng roots rich in ginsenosides Rb1 and Rg1 with dammarane-type aglycone. This is the first report to declare the distribution of ginsenosides in underground parts of wild P. ginseng. Ginsenoside Ro is a minor ginsenoside in ginseng whereas it is the major ginsenoside in P. japonicus rhizome (chikusetsu-ninjin in Japanese). Ginsenoside Ro is characterized by antiinflammatory effects which differ from ginsenosides Rb1 and Rg1 responsible for adaptogenic effects of ginseng. These results suggest that "Rozu" containing both oleanane- and dammarane-type ginsenosides might be a promising raw material distinct from ginseng root or P. japonicus rhizome.     

Anxiolytic-like effects of ginsenosides on the elevated plus-maze model in mice

In a previous study, we reported that ginseng extract has anxiolytic-like effects in the elevated plus-maze model and that the ginseng saponin fraction plays an important role. This experiment was performed to investigate the anxiolytic-like effects of ginsenosides Rb1, Rg1, Rg3-R, and Rg3-S, and the Rg5 and Rk mixture isolated from the ginseng saponin fraction in the elevated plus-maze. Furthermore, the anxiolytic-effects of Rb1, Rg1, Rg3-R, Rg3-S, and the Rg5 and Rk mixture were compared with those of a well-known active anxiolytic drug (diazepam). The oral administration of ginsenoside Rb1 significantly increased the number of open arm entries and the time spent on the open arm compared with those in the vehicle-treated group. Ginsenoside Rg1 and the Rg5 and Rk mixture also significantly increased the number of open arm entries and the time spent on the open arm. However, ginsenosides Rg3-R and Rg3-S did not increase the number of open arm entries or the time spent on the open arm. On the other hand, ginsenoside Rb1 and the Rg5 and Rk mixture decreased locomotor activity in a manner similar to diazepam. These data indicate that ginsenosides Rb1, Rg1, and the Rg5 and Rk mixture have anxiolytic-like effects, but ginsenosides Rg3-R and Rg3-S do not in this model. We provide evidence that some ginsenosides may be useful for the treatment of anxiety.