About Bioline  All Journals  Testimonials  Support Bioline  News

Iranian Journal of Pharmacology and Therapeutics
Razi Institute for Drug Research (RIDR) of Iran University of Medical Sciences and Health Services (IUMS)
ISSN: 1735-2657
Vol. 3, Num. 2, 2004, pp. 30-40

Iranian Journal of Pharmacology & Therapeutics, Vol. 3, No. 2, 2004, pp. 30-40

Use of Ginseng in Medicine: Perspectives on CNS Disorders

Khaled Radad, Gabriele Gille and Wolf-Dieter Rausch

Department of Pathology, Faculty of Veterinary Medicine, Assiut University, Assiut, Egypt (K.R.); Department of Neurology, Technical University, Dresden, Germany (G.G.); Institute for Medical Chemistry, Veterinary Medical University, Vienna, Austria (W.R.)
Address correspondence to: Prof. Dr. Wolf-Dieter Rausch, Institute for Medical Chemistry, Veterinary Medical University Vienna, Veterinaerplatz 1, A-1210 Vienna, Austria. E-mail:

Received August 22, 2004;
Revised October 6, 2004;
Accepted October 12, 2004

Code Number: pt04005


Ginseng, the root of Panax species, is a well-known folk medicine. It has been used as traditional herbal medicine in China, Korea and Japan for thousands of years and today is a popular and worldwide used natural medicine. The active ingredients of ginseng are ginsenosides which are also called ginseng saponins. Recently, there is increasing evidence in the literature on the pharmacological and physiological actions of ginseng. Ginseng had been used primarily as a tonic to invigorate week bodies and help the restoration of homeostasis. However current in vivo and in vitro studies have shown its beneficial effects in a wide range of pathological conditions such as cardiovascular diseases, cancer, immune deficiency and hepatotoxicity. Moreover, recent research has suggested that some of ginseng’s active ingredients also exert beneficial actions on aging, CNS disorders and neurodegenerative diseases. In general, antioxidant, anti-inflammatory, anti-apoptotic and immunostimulant activities are mostly underlying the possible ginseng-mediated protective mechanisms. Next to animal studies, data from neural cell cultures contribute to the understanding of these mechanisms which involve decreasing nitric oxide (NO), scavenging of free radicals and counteracting excitotoxicity. In this review we focus on recently reported medicinal effects of ginseng and summarize the current knowledge of its effects on CNS disorders and neurodegenerative diseases.

Keywords: Ginseng, Ginsenosides, CNS, Medicine, Chinese herbs

Ginseng refers to the root of several species in the plant genus Panax (C. A. Meyer Araliaceae). Among them, Panax ginseng is the most widely used ginseng and is indigenous to the Far East countries (most notably China and Korea). Panax ginseng was first cultivated around 11 BC and has a medical history of more than five thousand years. The genus name of Panax ginseng “Panax” was given by the Russian botanist, C.A. Meyer, and is derived from the Greek words “pan” meaning all and “axos” meaning cure. The species name “ginseng” comes from the Chinese word “rensheng” which means “human” as ginseng root resemble the human body [1]. In China, ginseng roots are harvested when the plant is 3-6 years old and then, the roots are submitted to air drying (white ginseng) or are steamed (red ginseng). Interestingly, after these two ways of treatment the roots differ in their content of saponins [1] and this may be the reason for the variable actions of different ginseng products. Other species of the genus Panax include Panax quinquefolius (found in southern Canada and in the United States), Panax japonicus (grown in Japan), and less frequently Panax notoginseng (grown in China), Panax pseudoginseng (grown in Nepal and eastern Himalayas) and Panax vietnamensis (grown in Vietnam) [2].

Ginseng is a widespread herbal medicine [3] and it has served as an important component of many Chinese prescriptions for thousands of years [4, 5]. Today it still occupies a permanent and prominent position in the herbal (best-sellers) list and is considered the most widely taken herbal product in the world [6]. Moreover, it is estimated that more than six million Americans are regularly consuming ginseng products [7]. They do not only believe that ginseng will engender physical benefits, but that it will also have positive effect on their cognitive performance and well-being.

Ginsenosides or ginseng saponins are the principle active ingredients in ginseng and more than thirty different ginsenosides have been identified [8, 9]. Ginsenosides are unique to Panax species, many of which exist in minute amounts and are believed to be responsible for most of ginseng’s actions [10-13]. Additionally, ginsenosides operate by many mechanisms of action and it was suggested that each ginsenoside may have its own specific tissue-dependent effects [14]. The basic structure of ginsenosides is similar. They consist of a gonane steroid nucleus with 17 carbon atoms arranged in four rings. The characteristic biological responses for each ginsenoside are attributed to the differences in the type, position and number of sugar moieties attached by glicosidic bond at C-3 and C-6 [15]. Based on their structural differences, they can be classified into three categories: the panaxadiol group (e.g. Rb1, Rb2, Rb3, Rc, Rd, Rg3, Rh2, Rs1), the panaxatriol group (e.g. Re, Rf, Rg1, Rg2, Rh1), and the oleanolic acid group (e.g. Ro) [5, 16]. Interestingly, the ginsenoside content of ginseng can vary depending on the Panax species, the plant age, the part of the plant, the preservation method, the season of harvest and the extraction method [17, 18].

Nowadays, herbal medicines have received great importance and are recommended as natural alternatives to maintain one’s health. Therefore, in this review we try to focus on the recently reported medicinal effects of ginseng and to summarize the results of different scientific studies using ginseng particularly in CNS disorders.

General Effects of Ginseng

Ginseng products are usually used as general tonic and adaptogen to help the body to resist the adverse influences of a wide range of physical, chemical and biological factors and to restore homeostasis [1, 19]. These tonic and adaptogenic effects of ginseng are believed to enhance physical performance (including sexual function) and general vitality in healthy individuals, to increase the body’s ability to fight stress in stressful circumstances and to support resistance to diseases by strengthening normal body function as well as to reduce the detrimental effects of the aging processes [12, 20].

Neuropharmacology of Ginseng

Ginseng rescues neuronal cells either in vivo or in vitro

Recently, it has been shown that ginseng and its components, ginsenosides, have a wide range of actions in the central nervous system [21]. These effects include increased cell survival, extension of neurite growth and rescuing of neurons from death due to different insults either in vivo or in vitro. Sugaya et al. [22], Himi et al. [4] and Mizumaki et al. [23] reported that ginseng roots appeared to facilitate survival and neurite extension of cultured cortical neurons and Kim et al. [24] showed that ginsenosides Rb1 and Rg3 protected neurons from glutamate-induced neurotoxicity. Following forebrain ischemia in gerbils, Wen et al. [5] and Lim et al. [25] demonstrated that central infusion of ginsenoside Rb1 rescued the hippocampal CA1 neurons against lethal damage of cellular hypoxia. Using a spinal neuron model, ginsenosides Rb1 and Rg1 proved to be potentially effective therapeutic agents for spinal cord injuries as they protected spinal neurons from excitotoxicity induced by glutamate and kainic acid, and oxidative stress induced by hydrogen peroxide [26].

Ginseng’s role in Parkinson’s disease models

A number of studies have recently described the beneficial effect of ginseng and its main components, ginsenosides, on some neurodegenerative disease models. Special interest has been paid to Parkinson’s disease (PD) models either in vivo or in vitro. In an in vivo model, Van Kampen et al. [21] reported that prolonged oral administration of ginseng extract G115 significantly protected against neurotoxic effects of parkinsonism-inducing agents such as 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and its active metabolite 1-methyl-4-phenylpyridinium (MPP+) in rodents. He found that ginseng-treated animals sustained less damage and TH+ neuronal loss in substantia nigra pars compacta (SNpc) after MPP+ exposure. Likewise reduction of TH immunoreactivity in striatum was effectively diminished as a result of ginseng treatment compared to MPP+ exposed animals. Similarly, striatal dopamine transporter (DAT) was significantly preserved due to ginseng treatment. In in vitro studies, it has been shown that ginseng saponins enhanced neurite growth of the dopaminergic SK-N-SH neuroblastoma cells [27]. As mentioned above, we showed recently that ginsenosides Rb1 and Rg1 increased the survival of primary cultured dopaminergic cells and promoted their neuritic growth after exposure to either MPP+ or glutamate [28, 29] (Fig 1 , 2, 3). Interestingly, Tanner and Ben-Schlomo [30] speculated that geographic variations in PD prevalence might reflect ginseng consumption as in North America, PD occurs in approximately 200 cases per 100,000 persons compared to only 44 cases per 100,000 in China. On the other hand, this variation in PD prevalence in different populations may strengthen the familial theory of PD rather than consumption of ginseng.

Although the processes and mechanisms underlying the neuroprotective effects of ginseng upon dopaminergic neurons remain to be elucidated several reports demonstrate the inhibitory role of ginseng on MPP+ uptake in dopaminergic neurons, the suppression of oxidative stress induced by autooxidation of dopamine, the attenuation of MPP+-induced apoptosis and the potentiation of nerve growth factor (NGF). It has been shown that certain ginsenosides inhibit dopamine uptake into rat synaptosomes [31] and consequently ginseng could potentially provide protection against MPP+ through blockade of its uptake by dopaminergic neurons [21]. Ginsenoside Rg1 could interrupt dopamine-induced elevation of reactive oxygen species (ROS) or NO generation in pheochromocytoma cells (PC12) [32]. Kim et al. [33] and Chen et al. [34] reported that Ginseng radix attenuated MPP+-induced apoptosis as it decreased the intensity of MPP+-induced DNA laddering in PC12 cells and ginsenoside Rg1 had protective effect against MPTP-induced apoptosis in the mouse substantia nigra. This anti-apoptotic effect of ginseng may be attributed to enhanced expression of Bcl-2 and Bcl-xl, reduced expression of bax and nitric oxide synthase (NOS) and inhibited activation of caspase-3. Ginseng may also reverse the neurotoxic effects of MPP+ through elevation of NGF mRNA expression [21]. In accordance, Salim et al. [35] showed that ginsenosides Rb1 and Rg1 elevate NGF mRNA expression in rat brain and Rudakewich et al. [36] concluded that both ginsenosides potentiate NGF-induced neurite outgrowth in cell culture.  Furthermore, it has been reported that ginsenosides Rb1, Rg1, Rc and Re inhibited tyrosine hydroxylse activity and exhibited anti-dopaminergic action since they reduced the availability of dopamine at presynaptic dopamine receptors [37].

There are few reports concerning the effect of ginseng on the other neurodegenerative diseases. Jiang et al. [38] and Lee et al. [39] reported that ginseng and its components prevent neuronal loss in amyotrophic lateral sclerosis models and Ginseng radix has been used for treatment of various neurodegenerative disorders including Alzheimer’s disease, respectively.

General mechanisms and processes underlying neuropharmacology of ginseng

In addition to the mechanisms involved in neuroprotection of dopaminergic neurons, there exist additional data demonstrating the protective potential of ginseng against various neuronal insults. Potentiation of NGF by ginseng is also involved in other neuronal models. Nishiyama et al. [40] and Liao et al. [26] reported that ginsenosides increased neuronal survival and promoted neurite outgrowth of cultured chick embryonic dorsal root ganglia and cultured spinal cord neurons, respectively. Moreover, ginsenosides alleviated oxidative stress by scavenging of free radicals, inhibited NO production which usually  accompanies glutamate excitotoxicity, induced superoxide dismutase (SOD1) and catalase genes and reduced lipid peroxidation [24, 41-43]. Also, it has been suggested that ginseng, in particular ginsenoside Rg3, inhibits both N-methyl-D-aspartate (NMDA) and non-NMDA glutamate receptors [44, 45] which contribute significantly to most neurological disorders [46-48]. Inhibition of NMDA and non-NMDA receptors by ginsenosides resulted in a reduction of Ca2+ over-influx into neurons and thus protected cells from neurodegenerative processes evoked by Ca2+ overload [26, 49]. These findings are in line with our results in a recent study since we found that ginsenosides Rb1 and Rg1 increased red/green fluorescence ratio of mitochondrial JC-1 staining in primary dopaminergic cell culture after glutamate treatment indicating the possible role of both ginsenosides in attenuating mitochondrial depolarization induced by glutamate excitotoxicity and subsequent Ca2+ over-influx into mitochondria [28]. Additionally, inhibition of Na+ channel [50] and improved energy metabolism by retarding ATP breakdown in cultured neurons and preservation structural integrity are also involved [51]. Furthermore, few reports showed that neuroprotection by ginseng may be, in part, due to its effect on glial populations. In this respect, it has been reported that ginseng total saponins prevent astrocytes swelling induced by glutamate [52] and ginsenoside Rg1 inhibited microglial respiratory burst activity and decreased the accumulation of NO produced by activated microglia [53].

Modulatory effect of ginseng on neurotransmission

A number of studies have shown that some ginsenosides can modulate neurotransmission in the brain. Both ginsenosides Rb1 and Rg1, the most abundant ginsenosides in ginseng root, can modulate acetylcholine release and re-uptake and the number of choline uptake sites especially in the hippocampus [54]. They also increase choline acetyltransferase levels in rodent brains [35, 55]. These results suggested that these compounds may improve central cholinergic function in humans and may be used to treat memory deficit [36]. It has also been reported that ginsenosides increased dopamine and norepinephrine in cerebral cortex [56] which may explain the favorable effects of ginseng extract upon attention, cognitive processing, integrated sensory-motor function and auditory reaction time in healthy subjects [57]. Additionally, it has been shown that ginseng total saponins can modulate dopaminergic activity at both pre-synaptic and post-synaptic receptors [58], and can block behavioral sensitization induced by psychostimulants such as morphine [59], cocaine [58], methamphetamines [60] and nicotine [61-63]. Furthermore, it was found that ginseng increased serotonin in the cortex [64], ginseng saponins raised the levels of biogenic amines in normal rat brain [65], ginsenoside Rg2 directly interacted with nicotinic receptor subtypes [66] and ginseng administration lead to regulation of GABAergic transmission in animals [67, 68].

Cognitive effects of ginseng

The use of herbal medicine, particularly ginseng, for improving cognitive performance has become increasingly popular during recent years and some studies have shown its enhancing effects on learning and memory either in aged and/or brain damaged individuals [69, 70]. For example, significant improvement in learning and memory has been observed in aged and brain-damaged rats after local administration of ginseng powder [71-73]. In humans, Terasawa et al. [74] and D’Angelo et al. [57] have shown that ginseng or ginseng extract had significant effects on neurological and psychiatric symptoms in aged humans and psychomotor functions in healthy subjects respectively. This positive effect of ginseng on cognition performance is owing to the direct action of ginseng on the hippocampus [75]. Consistent with the study of Kurimoto et al. [75], Wen et al. [5] demonstrated that red ginseng, ginseng powder and ginsenoside Rb1 administration for seven days prior to ischaemia rescued the hippocampal CA1 pyramidal neurons and subsequently ameliorated learning deficits in gerbils. Moreover, Shen and Zhang [76] suggested that the influence of ginsenoside Rg1 on the proliferating ability of neuronal progenitors may serve as an important mechanism underlying its nootropic and anti-aging effects particularly on learning and memory.

On the other hand, Persson et al. [77] have reported in a more recent study that regular use of ginseng during long period of time (up to 2 years) by healthy participants did not provide any quantifiable beneficial effects on memory performance. This result coincides with the finding of Sorensen and Sonne [78] who reported that ginseng intake did not enhance memory functions.

Table 1. Important ginseng’s effects and its possible actions on different body’ systems


Ginseng’s effect(s)

  Possible action(s)

Whole body

General tonic and adaptogen


·          Resistance against adverse conditions (physical, chemical and biological factors)

·          Restores body’s homeostasis

·          Anti-aging effects


Central Nervous system

Neuroprotection either in vivo or in vitro


·          Potentiates nerve growth factor

·          Anti-oxidative and anti-apoptotic mechanisms

·          Reduces lipid peroxidation

·          Inhibits excitotoxicity and Ca2+ over-influx into neurons

·          Maintains cellular ATP levels

·          Preserves structural integrity of neurons



Glial cells


·          Prevents astroglial swelling

·          Inhibits microglial respiratory burst activity and NO production by activated microglia



Increasing cognitive performance (learning & memory)



·          Modulates neurotransmission

·          Direct effect on hippocampal neurons


Cardiovascular system



·          Relaxes vascular smooth muscle cells through NO and Ca2+ mediated mechanisms

·          Inhibits production of endothelin which plays a role in blood vessel constriction



Anti-atherosclerotic effect


·          Prevents platelet aggregation

·          Shows antagonistic action for platelet activity factor

·          Suppresses thrombin formation



Acceleration of wound healing


·          Promotes functional neovascularization through endothelial proliferation


Inflammation and allergy

Anti-inflammatory and anti-allergic effects


·          Inhibits cytokine production such as IL-1β, IL-6 and TNF-α

·          Abrogates cyclooxygenase -2 gene expression

·          Suppresses histamine and leukotrienes release from mast cells

·          Stabilizes inflammatory cells such as neutrophils and lymphocytes

·          Antifibroblastic activity


Immune system



·          Enhances interferon induction, phagocytosis, natural killer cells, and B and T cells



Anti-carcinogenic effect


·          Suppresses malignant transformation

·          Inhibits proliferation of tumor cells

·          Inhibits tumor invasiveness, metastasis and angiogenesis


Aphrodisiac effect

Enhancement of male copulatory behavior


·          Relaxes corpus cavernosum smooth muscles via NO mediated processes

·          Increases serum testosterone levels and reduces plasma levels of prolactin hormone

·          Direct effects on anterior pituitary and hypothalamic dopaminergic mechanisms



Antihyperglycemic activity


·          Increases plasma insulin levels, the number of insulin receptors and insulin sensitivity





Cardiovascular Effects of Ginseng

Ginseng has been shown to produce a number of actions on the cardiovascular system. Intravenous administration of ginseng to anaesthetized dogs resulted in reduction, followed by an increase in blood pressure, and transient vasodilatation [79]. In rats and rabbits, Lei and Chiou [80] and Kim et al. [81] found that extracts of Panax notoginseng decreased systemic blood pressure and ginsenosides exerted relaxing effects in rings of rat and rabbit aorta, respectively. This relaxing effect of ginseng and its active constituents on the cardiovascular system is partially due to the release of endothelial NO. Researchers have reported that chronic feeding of rabbits with ginsenosides may enhance indirectly vasodilatation by preventing NO degradation by oxygen radicals such as superoxide anions [82]. Ginsenosides have depressant action on cardiomyocyte contraction which may be mediated, in part, through increased NO production [83]. Korean red ginseng can improve the vascular endothelial dysfunction in patients with hypertension possibly through increasing NO [84]. In addition to endothelium-derived NO release, Li et al. [85] reported that ginsenosides-induced vasorelaxation also involves Ca2+ activated K+ channels in vascular smooth muscle cells.

It has also been reported that crude saponin fractions of Korean red ginseng enhanced cerebral blood flow in rats [86] and ginsenosides reduced plasma cholesterol levels and the formation of atheroma in the aorta of rabbits fed on a high cholesterol diet [82]. This antiatherosclerotic action of ginseng components is apparently due to the correction in the balance between prostacyclin and thromboxane [87], inhibition of 5-hydroxytryptamine (5-HT) release from, and adrenaline and thrombin-induced aggregation of platelets [88], regulation of cGMP and cAMP levels and prolongation of the time interval between conversions of fibrinogen to fibrin [89]. Also, ginsenosides have been shown to be relatively potent platelet activating factor antagonist [90]. In parallel with these findings, Nakajima et al. [91] found red ginseng to promote the proliferation of vascular endothelial cells, to inhibit the production of endothelin which is known to constrict blood vessels resulting in raising blood pressure and to increase the production of interleukin 1 beta, which suppresses the formation of thrombin in blood coagulation. In the same direction, Yuan et al. [92] used cultured human umbilical vein endothelial cells to conclude that American ginseng, Panax quinquefolium L. extracts, significantly decreased endothelin concentration in a dose and time dependent manner after thrombin treatment.

The role of ginseng in angiogenesis has also been studied. Ginsenoside Rg1 promoted functional neovascularization into a polymer scaffold in vivo and tubulogenesis by endothelial cells in vitro [93]. Therefore, ginsenoside Rg1 might be useful in wound healing as it can induce therapeutic angiogenesis.

Anti-Inflammatory and Anti-Allergic Effects of Ginseng

More recently, the role of ginseng in modulation of inflammatory and allergic processes has been documented by some researchers. For example, Ginseng root saponins exerted an inhibitory effect on IL-1β and IL-6 gene expression in a chronic inflammation model of aged rats, ginsenosides Rb1 and Rg1 decreased TNF-α production by murine macrophages, pretreatment with ginsenoside Rg3 abrogated cyclooxygenase-2 expression in response to 12-0-tetradecanoylphorbol-13-acetate (TPA) in mice skin and ginsenosides Rb1 and Rc suppressed histamine and leukotrienes release during the activation of guinea pig lung mast cells in vitro [94-97]. An additional anti-inflammatory action by ginseng has been mentioned by Li and Li [98]. They reported that total saponins of Sanchi (Panax pseudo-ginseng notoginseng) reduced the level of the intracellular Ca2+ concentration in neutrophils and Kim et al. [99] found that ginseng had radioprotective effect against γ-ray-induced DNA double strand breaks in cultured murine spleen lymphocytes. Furthermore, it was found that ginseng promoted apoptosis in renal interstitial fibroblasts and thus could affect renal interstitial fibrosis [100]. Ginseng also has immunostimulant effects as it enhances interferon induction, phagocytosis, natural killer (NK) cell, and B and T cells in various animal species including mice and guinea pigs and also in humans [101-104]. Hu et al. [105] reported that ginseng stimulated the immune system of dairy cows as it activated the innate immunity of cows and contributed to the cow’s recovery from mastitis.

Anti-Carcinogenic Effect of Ginseng

Although some of ginseng’s activities against cancer have already been reviewed elsewhere, in this section we try to focus on the most common and recent findings related to the anti-cancer effect of ginseng. Researchers have reported that chronic intake of Panax ginseng C. A. Meyer decreased the incidence of cancers such as lung, gastric, liver and colorectal tumors [106, 107]. Ginsenoside Rh2 has been shown to suppress proliferation in a number of human cancer cells including breast, prostate, hepatic and intestinal cancer, but also in animal cell lines [108-111]. Ginsenosides Rb1, Rb2 and Rc inhibited tumor angiogenesis and metastasis [112] while ginsenoside Rh1 inhibited proliferation of the NIH 3T3 mouse fibroblast cell line [113].

Some of the mechanisms and processes underlying the former beneficial effects of ginseng against cancer have been stated by Surh et al. [114] and others. Using both in vivo and in vitro models, Surh et al [114] reported that ginsenoside Rg3 treatment caused marked suppression of TPA-induced cyclooxygenase-2 (COX-2) expression in mouse skin and in human breast epithelial cells (MCF-10A). Also, he observed the same suppressive effect on NF-kB in mouse skin and extracellular regulated protein kinases (ERK) activation in TPA-stimulated MCF-10A cells. Consistent with the results of Surh et al. [114], Keum et al. [115] reported that topical application of ginseng extract prior to each topical dose of the tumor promoter TPA markedly lowered the papilloma formation in mouse skin and caused substantial reduction in epidermal ornithine decarboxylase (ODC) activity and suppressed the expression of its mRNA. All of the above mentioned enzymes and factors are, in part, involved in tumorogenesis. COX-2 was upregulated in transformed cells and in various forms of cancer. Its overexpression inhibited apoptosis and increased the invasiveness of tumor cells [116]. ODC is a rate-limiting enzyme in the biosynthesis of polyamines that play a pivotal role in cell proliferation and tumor promotion [117]. Mitogen-activated protein kinase (MAPK) cascade is responsible, in part, for upregulation of COX-2 as specific inhibitors of the corresponding MAPK abolish the induction of COX-2 and result in production of prostaglandin E2 [114]. NF-κB is a ubiquitous eukaryotic transcription factor implicated in cellular proliferation and malignant transformation. Its activation is an essential early event prior to malignant transformation by inhibiting cell death signal activated by oncogenic Ras [118].

Aphrodisiac Effect of Ginseng

Ginseng effects on sex behavior have been discussed recently by Murphy et al. [119], Nocerino et al. [1] and Murphy and Lee [14]. In brief, it has been shown that ginseng is an essential constituent in traditional Chinese medicine for treatment of sexual impotence [1] and, Panax ginseng and Panax quinquefolium enhanced male copulatory behavior in rats [119, 120]. Consistent with these finding, Choi et al. [121] confirmed in a clinical study the efficacy of Korean red ginseng for erectile dysfunction in 30 patients. These positive aphrodisiac effects of ginseng may be attributed to the enhancement of nitric oxide release from endothelial cells of penile corpus cavernosum and consequent relaxation [122]. Furthermore, Fahim et al. [123] and Bahrke and Morgan [124] reported that Panax ginseng produced a dose-related increase in serum testosterone levels and American ginseng reduced the plasma level of prolactin hormone in rats. Testosterone might mediate the heightened copulatory behavior in ginseng-treated animals while, prolactin altered it. Taken together, these results suggest that both ginseng species may have direct actions on the anterior pituitary gland and/or on the hypothalamic dopaminergic mechanisms [14].

Other Pharmacological Effects of Ginseng

Ginseng and its constituents, ginsenosides, have a number of other pharmacological actions including antipyretic activity, increase of gastro-intestinal tract motility and acceleration of glycolysis and cholesterol synthesis as well as increased synthesis of serum protein (Fig 4 ) [36]. Another important biological effect reported for Panax ginseng or its saponins is hypoglycemic and antihyperglycemic activity [125, 126]. It has been shown that ginsenoside Rg1 increased the number of insulin receptors [127] and panaxan B, the main constituent of Panax ginseng for hypoglycemic activity, increased the plasma insulin level and enhanced insulin sensitivity [125]. Ginseng also shows anti-stress activities against physical (i), chemical (ii) and biological (iii) stressful circumstances. For instance: (i) it was shown that treatment with root saponins partially prevented the rectal temperature decline in normal rats exposed to cold stress [128], extracts of Panax ginseng had radioprotective effects or prolonged the survival time of irradiated mice [129, 130] and accelerated the hematological recovery of mice after x-ray irradiation [131] as well as reduced DNA damage in normal cells [132], (ii) ginseng can moderate chemical stress as it decreased damage to rat liver and inhibited the elevation of serum glutamic pyruvic transaminase in carbon tetrachloride or thioacetamide-intoxicated mice [133, 134] and (iii) Panax ginseng saponins-treated mice were found to be more resistant to infections by Staphylococcus aureus , Escherichia coli and Salmonella typhi [135], saponins attenuated the process of trypanosomiasis, prolonged the life span of the treated mice and delayed the appearance of trypanosomes in their blood [136]. It also prevented the development of fever induced by typhoid and paratyphoid vaccines. Moreover, the aqueous extract of ginseng radix produced beneficial effects against gastritis and ginsenoside Rb1 had anti-ulcer effect through increasing mucus secretion [137].

Adverse Effects and Drug Interaction of Ginseng

The root of Panax ginseng appeared nontoxic to rats, dogs and humans [138, 139]. In inappropriate use, the most commonly experienced symptoms are hypertension, diarrhea, sleeplessness, mastalgia, eruptions and vaginal bleeding [124, 140]. Additionally, Siegel [141] described the term ginseng abuse syndrome after studying 133 users in Los Angeles. He has indicated that the long term effects of the use of ginseng is characterized by hypertension, nervousness, sleeplessness, skin rash, diarrhea, confusion, depression or depersonalization. Possible drug interactions have been reported between Panax ginseng and warfarin, phenelzine and alcohol [140].

Concluding Remarks

To our understanding, the worldwide spread of ginseng as a medical herb and its intake by many healthy individuals to invigorate their bodies are based primarily on (i) its empirical history in contributing to the recovery from a wide rang of disease conditions particularly in the Far East countries and (ii) the results of recent experimental research which reported some of its beneficial effects in experimental animals. To date, there is a shortage in the literature concerning the clinical use of ginseng to treat certain diseases in patients. Also, further research has to be considered to elucidate the definite pharmacological actions of ginseng and its constituents.


  1. Nocerino E, Amato M, Izzo AA. The aphrodisiac and adaptogenic properties of ginseng. Fitoterapia 2000;71:1-5.

  2. Yun TK. Brief introduction of Panax ginseng C.A. Meyer. J Korean Med Sci 2001;16:53-55.

  3. Rhim H, Kim H, Lee DY, Oh TH, Nah SY. Ginseng and ginsenoside Rg3, a newly identical active ingredient of ginseng, modulate Ca2+ channel currents in rat sensory neurons. Eur J Pharmacol 2002;463:151-158.

  4. Himi T, Saito H, Nishiyama N. Effects of ginseng saponins on the survival of cerebral cortex neurons in cell cultures. Chem Pharm Bull (Tokyo) 1989;37:481-484.

  5. Wen TC, Yoshimura H, Matsuda S, Lim JH, Sakanaka M. Ginseng root prevents learning disability and neuronal loss in gerbils with 5-minute forebrain ischaemia. Acta Neuropathol 1996;91:15-22.

  6. Blumenthal M. Asian ginseng: potential therapeutic uses. Adv Nurse Pract 2001;2:26-28.

  7. Smolinski AT, Pestka JJ. Modulation of lipopolysacchride-induced proinflammatory cytokine production in vitro and in vivo by the herbal constituents apigenin (chamomile), ginsenoside Rb1 (ginseng) and parthenolide. Food and Chem Toxicol 2003;41:1381-1390.

  8. Liu CX, Xiao PG. Recent advances on ginseng research in China. J Ethnopharmacol 1992;36:27-38.

  9. Back NI, Kim DS, Lee YH, Park JD, Lee CB, Kim SI. Ginsenoside Rh4, a genuine dammarane glycoside from korean red ginseng. Planta Med 1996;62:86-87.

  10. Attele AS, Wu JA, Yuan CS. Ginseng pharmacology: multiple constituents and multiple actions. Biochem Pahrmacol 1999;58:1685-1693.

  11. Fleming T. Physician desk references for herbal medicine. First ed Medical Economics Company, Montvale, NJ, 1998.

  12. Tyler VE. The Honest Herbal-A Sensible Guide to the Use of Herbs and Related Remedies. Third ed The Haworth Press, New York, 1993.

  13. Wakabayashi C, Hasegawa H, Murata J, Saiki I. In vivo antimetastatic action of ginseng protopanaxadiol saponins is based on their intestinal bacterial metabolism after oral administration. Oncology Res 1997;9:411-417.

  14. Murphy LL, Lee TJ. Ginseng, sex behavior and nitric oxide. Ann NY Acad Sci 2002;962:372-377.

  15. Byun BH, Shin I, Yoon YS, Kim SI, Joe CO. Modulation of protein kinase C activity in NIH 3T3 cells by plant glycosides from Panax ginseng. Planta Med 1997;63:389-392.

  16. Tackikawa E, Kudo K, Harada K, Kashimoto T, Miyate M, Kakizaki A. Effects of ginseng saponins on responses induced by various receptor stimuli. Eur J Pharmacol 1999;369:23-32.

  17. Liberti LE, Der Mardersian A. Evaluation of commercial ginseng products. J Pharm Sci 1978;10:1487-1489.

  18. Phillipson JD, Anderson LA. Ginseng-quality safety and efficacy? Pharm J 1984;232:161-165.

  19. Brekhman I, Dardymov I. New substances of plant origin which increase non specific resistance. Ann Rev Pharmacol 1969;9:419-430.

  20. O’Hara M, Kiefer D, Farrell K, Kemper K. A review of 12 commonly used medicinal herbs. Arch Fam Med 1998;7:523-536.

  21. Van Kampen J, Robertson H, Hagg T, Drobitch R. Neuroprotective actions of the ginseng extract G115 in two rodent models of Parkinson’s disease. Exp Neurol 2003;184:21-29.

  22. Sugaya A, Yuzurihara M, Tsuda T, Yasuda K, Kajiwara K, Sugaya AE. Proliferative effect of ginseng saponin on neurite extension of primary cultured neurons of the rat cerebral cortex. J Ethnopharmacol 1988;22:173-181.

  23. Mizumaki Y, Kurimoto M, Hirashima Y, Nishijima M, Kamiyama H, Nagai S, Takaku A, Sugihara K, Shimizu M, Endo S. Lipophilic fraction of Panax ginseng induces neuronal differentiation of PC12 cells and promotes neuronal survival of rat cortical neurons by protein kinase C dependent manner. Brain Res 2002;20:254-260.

  24. Kim YC, Kim SR, Markelonis GJ, Oh TH. Ginsenosides Rb1 and Rg3 protect cultured rat cortical cells from glutamate-induced neurodegeneration. J Neurosci Res 1998;4:426-432.

  25. Lim JH, Wen TC, Matsuda S, Tanaka J, Maeda N, Peng H, Aburaya J, Ishihara K, Sakanaka M. Protection of ischaemic hippocampal neurons by ginsenosides Rb1, a main ingredient of ginseng root. Neurosci Res 1997;28:191-200.

  26. Liao B, Newmark H, Zhou R. Neuroprotective effects of ginseng total saponin and ginsenosides Rb1 and Rg1 on spinal cord neurons in vitro. Exp Neurol 2002;173:224-234.

  27. Tohda C, Matsumoto N, Zou K, Meselhy MR, Komatsu K. Axonal and dendritic extension by protopanaxadiol-type saponins from ginseng drugs in SK-N-SH cells. Jpn J Pharmacol 2002;90:254-262.

  28. Radad K, Gille G, Moldzio R, Saito H, Rausch WD. Ginsenosides Rb1 and Rg1 effects on mesencephalic dopaminergic cells stressed with glutamate. Brain Res 2004;17:41-53.

  29. Radad K, Gille G, Moldzio R, Saito H, Ishige K, Rausch WD. Ginsenosides Rb1 and Rg1 effects on survival and neurite growth of MPP+-affected mesencephalic dopaminergic cells. J Neural Transm 2004;111:37-45.

  30. Tanner CM, Ben-Schlomo Y. Epidemiology of Parkinson’s disease. Adv Neurol 1999;80:153-159.

  31. Tsang D, Yeung HW, Tso WW, Peck H. Ginseng saponins: influence on neurotransmitter uptake in rat brain synaptosomes. Planta Med 1985;3:221-224.

  32. Chun CX, Gui ZY, An ZL, Chun H, Ying C, Min CL, Fang F, Can ZY, Hui ZC. Ginsenoside Rg1 attenuates dopamine-induced apoptosis in PC12 cells by suppressing oxidative stress. Eur J Pharmacol 2003;473:1-7.

  33. Kim EH, Jang MH, Shin MC, Shin MS, Kim CJ. Protective effect of aqueous extract of Ginseng radix against 1-methyl-4-phenylpyridinium-induced apoptosis in PC12 cells. Biol Pharm Bull 2003;26:1668-1673.

  34. Chen XC, Chen Y, Zhu YG, Fang F, Chen LM. Protective effect of ginsenoside Rg1 against MPTP-induced apoptosis in mouse substantia nigra neurons. Acta Pharmacol Sin 2002;23:829-834.

  35. Salim KN, McEven BS, Choa HM. Ginsenoside Rb1 regulates ChAT, NGF and trkA mRNA expression in the rat brain. Brain Res Mol Brain Res 1997;47:177-182.

  36. Rudakewich M, Ba F, Benishin CG. Neurotrophic and neuroprotective actions of ginsenosides Rb1 and Rg1. Planta Med 2001;67:533-537.

  37. Kim HS, Zhang YH, Fang LH, Lee MK. Effects of ginsenosides on bovine adrenal tyrosine hydroxylase. J Ethnopharmacol 1999;66:107-111.

  38. Jiang F, DeSilva S, Turnbull J. Beneficial effect of ginseng root in SOD-1 (G93A) transgenic mice. J Neurol Sci 2000;180:52-54.

  39. Lee TF, Shiao YJ, Chen CF, Wang LC. Effect of ginseng saponins on beta-amyloid-suppressed acetylcholine release from rat hippocampal slices. Planta Med 2001;67:634-637.

  40. Nishiyama N, Cho SI, Kitagawa I, Saito H. Malonylginsenoside Rb1 potentiates nerve growth factor (NGF)-induced neurite outgrowth of cultured chick embryonic dorsal root ganglia. Biol Pharm Bull 1994;17:509-513.

  41. Braughler JM, Chase RL, Neff GL, Yonkers PA, Day JS, Hall ED, Sethy VH, Lahti RA. A new 21-aminosteroid antioxidant lacking glucocorticoid activity stimulates adrenocorticotropin secretion and blocks arachidonic acid release from mouse pituitary tumor (AtT-20) cells. J Pharmacol Exp Ther 1988;244:423-427.

  42. Chu GX, Chen X. Anti-lipid peroxidation and protection of ginsenosides against cerebral ischemia-reperfusion injuries in rats. Zhongguo Yao Li Xue Bao 1990;11:119-123.

  43. Chang MS, Lee SG, Rho HM. Transcriptional activation of Cu/Zn superoxide dismutase and catalase genes by panaxadiol ginsenosides extracted from Panax ginseng. Phytother Res 1999;13:641-644.

  44. Kim S, Ahn K, Oh TH, Nah SY, Rhim H. Inhibitory effect of ginsenosides on NMDA receptor-mediated signals in rat hippocampal neurons. Biochem Biophys Res Commun 2002;296:247-254.

  45. Kim S, Rhim H. Ginsenosides inhibit NMDA receptor-mediated epileptic discharges in cultured hippocampal neurons. Arch Pharm Res 2004;27:524-530.

  46. Coyle JT, Puttfarcken P. Oxidative stress, glutamate, and neurodegenerative disorders. Science 1993;262:689-695.

  47. Choi DW, Rothman SM. The role of glutamate neurotoxicity in hypoxic-ischemic neuronal death. Annu Rev Neurosci 1990;13:171-182.

  48. Sattler R, Tymianski M. Molecular mechanisms of calcium-dependent excitotoxicity. J Mol Med 2000;78:3-13.

  49. Liu M, Zhang J. Effects of ginsenoside Rb1 and Rg1 on synaptosomal free calcium level, ATPase and calmodulin in rat hippocampus. Chin Med J 1995;108:544-547.

  50. Liu D, Li B, Liu Y, Attele AS, Kyle JW, Yuan CS. Voltage-dependent inhibition of brain Na+ channels by American ginseng. Eur J Pharmacol 2001;413:47-54.

  51. Jiang KY, Qian ZN. Effects of Panax notoginseng saponins on posthypoxic cell damage of neurons in vitro. Zhongguo Yao Li Xue Bao 1995;16:399-402.

  52. Seong YH, Shin CS, Kim HS, Baba A. Inhibitory effect of ginseng total saponins on glutamate-induced swelling of cultured astrocytes. Biol Pharm Bull 1995;18:1776-1778.

  53. Gong YS, Zhang JT. Effect of 17-beta-estradiol and ginsenoside Rg1 on reactive microglia induced by beta-amyloid peptides. J Asian Nat Prod Res 1999;1:153-161.

  54. Benishin CG. Actions of ginsenoside Rb1 on choline uptake in central cholinergic nerve endings. Neurochem Int 1992;21:1-5.

  55. Zhang JT, Qu ZW, Liu Y, Deng HL. Preliminary study on antiamnestic mechanism of ginsenosides Rb1 and Rg1. Chin Med J 1990;103:932-938.

  56. Itoh T, Zang YF, Murai S, Saito H. Effects of Panax ginseng root on the vertical and horizontal motor activities and on brain monoamine-related substances in mice. Planta Med 1989;55:429-433.

  57. D’Angelo L, Grimaldi R, Caravaggi M, Marcoli M, Perucca E, Lecchini S, Frigo GM, Crema A. A double-blind, placebo-controlled clinical study on the effect of a standardized ginseng extract on psychomotor performance in healthy volunteers. J Ethnopharmacol 1986;16:15-22.

  58. Kim HS, Kang JG, Seong YH, Nam KY, Oh KW. Blockade by ginseng total saponins of the development of cocaine induced reverse tolerance and dopamine receptor supersensitivity in mice. Pharmacol Biochem Behav 1995;50:23-27.

  59. Kim HS, Kang JG, Oh KW. Inhibition by ginseng total saponins of the development of morphine reverse tolerance and dopamine receptor supersensitivity in mice. Gen Pharmacol 1995;26:1071-1076.

  60. Kim HS, Hong YT, Oh KW, Seong YH, Rheu HM, Cho DH. Inhibition by ginsenosides Rb1 and Rg1 of methamphetamine-induced hypersensitivity, conditioned place preference and postsynaptic dopamine receptor supersensitivity on mice. Gen Pharmacol 1998;30:783-789.

  61. Kim HS, Kim K, Oh K. Ginseng total saponins inhibits nicotine induced hyperactivity and conditioned place preference in mice. J Ethnopharmacol 1999;66:83-90.

  62. Kim ND, Kang SY, Park JH, Schini-Kerth VB. Ginsenoside Rg3 mediates endothelium-dependent relaxation in response to ginsenoside in rat aorta: role of K+ channels. Eur J Pharmacol 1999;367:41-49.

  63. Shim I, Won J, Song J, Kim SE, Huh S. Modulatory effect of ginseng total saponins on dopamine release and tyrosine hydroxylase gene expression induced by nicotine in the mouse. J Ethnopharmacol 2000;70:161-169.

  64. Petkov V. Effect of ginseng on the brain biogenic monoamines and 3',5'-AMP system. Experiments on rats. Arzneimittelforschung 1978;28:388-393.

  65. Wang A, Cao Y, Wang Y, Zhao R, Liu C. Effects of Chinese ginseng root and stem-leaf saponins on learning, memory and biogenic monoamines of brain in rats. Zhongguo Zhong Yao Za Zhi 1995;20:493-495.

  66. Sala F, Mulet J, Choi S, Jung SY, Nah SY, Rhim H, Valor LM, Criado M, Sala S. Effects of ginsenoside Rg2 on human neuronal nicotinic acetylcholine receptors. J Pharmacol Exp Ther 2002;301:1052-1059.

  67. Kimura T, Saunders PA, Kim HS, Rheu HM, Oh KW, Ho IK. Interactions of ginsenosides with ligand-bindings of GABA(A) and GABA(B) receptors. Gen Pharmacol 1994;25:193-199.

  68. Choi SE, Choi S, Lee JH, Whiting PJ, Lee SM, Nah SY. Effects of ginsenosides on GABA(A) receptor channels expressed in Xenopus oocytes. Arch Pharm Res 2003;26:28-33.

  69. Yamaguchi Y, Higashi M, Kobayashi H. Effects of ginsenosides on impaired performance caused by scopolamine in rats. Eur J Pharmacol 1996;312:149-151.

  70. Mook-Jung I, Hong HS, Boo JH, Lee KH, Yun SH, Cheong MY, Joo I, Huh K, Jung MW. Ginsenoside Rb1 and Rg1 improve spatial learning and increase hippocampal synaptophysin level in mice. J Neurosci Res 2001;63:509-915.

  71. Zhao R, McDaniel WF. Ginseng improves strategic learning by normal and brain-damaged rats. Neuroreport 1998;11:1619-1624.

  72. Zhong YM, Nishijo H, Uwano T, Tamura R, Kawanishi K, Ono T. Red ginseng ameliorated place navigation deficits in young rats with hippocampal lesions and aged rats. Physiol Behav 2000;69:511-525.

  73. Kennedy DO, Scholey AB. Ginseng: potential for the enhancement of cognitive performance and mood. Pharmacol Biochem Behav 2003;75:687-700.

  74. Terasawa K, Shimada Y, Kita T. Choto-san in the treatment of vascular dementia: a double blind, placeb-controlled study. Phytomedicine 1997;4:15-22.

  75. Kurimoto H, Nishijo H, Uwano T, Yamaguchi H, Zhong YM, Kawanishi K, Ono T. Effects of nonsaponin fraction of red ginseng on learning deficits in aged rats. Physiol Behav 2004;82:345-355.

  76. Shen L, Zhang J. Ginsenoside Rg1 increases ischemia-induced cell proliferation and survival in the dentate gyrus of adult gerbils. Neurosci Lett 2003;344:1-4.

  77. Persson J, Bringlov E, Nilsson LG, Nyberg L. The memory-enhancing effects of Ginseng and Ginkgo biloba in healthy volunteers. Psychopharmacology 2004;172:430-434.

  78. Sorensen H, Sonne J. A double-masked study of the effect of ginseng on memory functions. Curr Ther Res 1996;57:959-968.

  79. Wood WB, Roh BL, White RP. Cardiovascular actions of Panax ginseng in dogs. Jpn J Pharmacol 1964;14:284-294.

  80. Lei XL, Chiou GC. Cardiovascular pharmacology of Panax notoginseng. Am J Chin Med 1986;14:145-152.

  81. Kim ND, Kang SY, Schini VB. Ginsenosides evoke endothelium-dependent vascular relaxation in rat aorta. Gen Pharmacol 1995;25:1071-1077.

  82. Kang SY, Kim SH, Schini VB, Kim ND. Dietary ginsenosides improve endothelium-dependent relaxation in the thoracic aorta of hypercholesterolemic rabbit. Gen Pharmacol 1995;26:483-487.

  83. Scott GI, Colligan PB, Ren BH, Ren J. Ginsenosides Rb1 and Re decrease cardiac contraction in adult rat ventricular myocytes: role of nitric oxide. Br J Pharmacol 2001;134:1159-1165.

  84. Sung J, Han KH, Zo JH, Park HJ, Kim CH, Oh BH. Effects of red ginseng upon vascular endothelial function in patients with essential hypertension. Am J Chin Med 2000;28:205-216.

  85. Li Z, Chen X, Niwa Y, Sakamoto S, Nakaya Y. Involvement of Ca2+ -activated K+ channels in ginsenosides-induced aortic relaxation in rats. J Cardiovasc Pharmacol 2001;37:41-47.

  86. Kim CS, Park JB, Kim KJ, Chang SJ, Ryoo SW, Jeon BH. Effect of Korea red ginseng on cerebral blood flow and superoxide production. Acta Pharmacol Sin 2002;23:1152-1156.

  87. Shi L, Fan PS, Wu L, Fang JX, Han ZX. Effects of total saponins of Panax notoginseng on increasing PGI2 in carotid artery and decreasing TXA2 in blood platelets. Zhongguo Yao Li Xue Bao 1990;11:29-32.

  88. Kimura Y, Okuda H, Arichi S. Effects of various ginseng saponins on 5-hydroxytryptamine release and aggregation in human platelets. J Pharm Pharmacol 1988;40:838-843.

  89. Park HJ, Lee JH, Song YB, Park KH. Effects of dietary supplementation of lipophilic fraction from Panax ginseng on cGMP and cAMP in rat platelets and on blood coagulation. Biol Pharm Bull 1996;19:1434-1439.

  90. Jung KY, Kim DS, Oh SR, Lee IS, Lee JJ, Park JD, Kim SI, Lee HK. Platelet activating factor antagonist activity of ginsenosides. Biol Pharm Bull 1998;21:79-80.

  91. Nakajima S, Uchiyama Y, Yoshida K, Mizukawa H, Haruki E. The effect of ginseng radius rubra on human vascular endothelial cells. Am J Chin Med 1998;26:365-373.

  92. Yuan CS, Attele AS, Wu JA, Lowell TK, Gu Z, Lin Y. Panax quinquefolium L. Inhibits thrombin-induced endothelin release in vitro. Am J Chin Med 1999;27:331-338.

  93. Sengupta S, Toh SA, Sellers LA, Skepper JN, Koolwijk P, Leung HW, Yeung HW, Wong RN, Sasisekharan R, Fan TP. Modulating angiogenesis: the yin and the yang in ginseng. Circulation 2004;7:1219-1225.

  94. Yu SC, Li XY. Effect of ginsenoside on IL-1 beta and IL-6 mRNA expression in hippocampal neurons in chronic inflammation model of aged rats. Acta Pharmacol Sin 2000;21:915-918.

  95. Cho JY, Park J, Yoo ES, Baik KU, Park MH. Effect of ginseng saponin on tumor necrosis factor-α production and T cell proliferation. Yakhak Hoeji 1998;43:296-301.

  96. Keum YS, Han SS, Chun KS, Park KK, Park JH, Lee SK, Surh YJ. Inhibitory effects of the ginsenoside Rg3 on phorbol ester-induced cyclooxygenase-2 expression, NF-kappaB activation and tumor promotion. Mutat Res 2003;523-524:75-85.

  97. Ro JY, Ahn YS, Kim KH. Inhibitory effect of ginsenoside on the mediator release in the guinea pig lung mast cells activated by specific antigen-antibody reactions. Int J Immunopharmacol 1998;20:625-641.

  98. Li X, Li SH. Effect of total saponins of Sanchi (Panax pseudo-ginseng notoginseng) on TNF, No and ist mechanisms. Chinese Traditional and herbal Drugs 1999;30:514-517.

  99. Kim TH, Lee YS, Cho CK, Park S, Choi SY, Yool SY. Protective effect of ginseng on radiation-induced DNA double strand breaks and repair in murine lymphocytes. Cancer Biother Radiopharm 1996;11:267-272.

  100. Zhang GQ, Ye RG, Kong QY, Yang NS, Zhang JL, Guan WM, Chen WM. Panax notoginseng saponins induced of human renal interstitial fibroblast and its mechanisms. Chin J Nephrology 1998;14:93-95.

  101. Matsuda H, Kubo M, Tani T, Kitagawa I, Mizuno M. Pharmacological study of Panax ginseng C. A. Meyer (IX). Protective effect of red ginseng on interferon (2) on phagocytic activity of mouse reticuloendothelial cells system. Shoyakugaku Zasshi 1987;41:135-131.

  102. Ahn YK, Kim YK, Chang JG, Kim JH, Goo JD. The effect of Korean ginseng on the immunotoxicity of mitomycin C. Yakhak Hoe Chi 1987;31:355-360.

  103. Park HW, Kim SC, Jung NP. The effect of ginseng saponin fractions on humoral immunity of mice. Korean J ginseng Sci 1988;12:63-67.

  104. Ohtani K, Mizutani K, kasai R. Reticuloendothelial system activating polysacchrides from Panax species: P. notoginseng, P. ginseng and P. japonicus. J Pharmacobio dyn 1987;10:63.

  105. Hu S, Concha C, Johannisson A, Meglia G, Waller KP. Effect of subcutaneous injection of ginseng on cows with subclinical Staphylococcus aureus mastitis. J Vet Med B Infect Dis Vet Public Health 2001;48:519-528.

  106. Yun TK. Experimental and epidemiologic evidence of cancer preventive effects of Panax ginseng C.A. Meyer. Nutr Rev 1996;54:71-81.

  107. Yun TK. Panax ginseng- a non-organ-specific cancer preventive? Lancet Oncol 2001;2:49-54.

  108. Lee YN, Lee HY, Chung HY, Kim SI, Lee SK, Park BC, Kim KW. In vitro induction of differentiation by ginsenoides in F9 teratocarcinoma cells. Eur J Cancer 1996;32:1420-1428.

  109. Park J, Lee KY, Oh YJ, Kim KW, Lee SK. Activation of caspase-3 protease via a Bcl-2-insensitive pathway during the process of ginsenoside Rh2-induced apoptosis. Cancer Lett 1997;121: 73-81.

  110. Oh M, Choi YH, Choi S, Chung H, Kim K, Kim SI, Kim DK, Kim ND. Anti-proliferating effects of ginsenoside Rh2 on MCF-7 human breast cancer cells. Int J Oncol 1999;14: 869-875.

  111. Kim HE, Oh JH, Lee SK, Oh YJ. Ginsenoside Rh2 induces apoptotic cell death in rat C6 glioma via a reactive oxygen- and caspase-dependent but Bcl-X(L)-independent pathway. Life Sci 1999;65:33-40.

  112. Mochizuki M, Yoo YC, Matsuzawa K, Sato K, Saiki I, Tono-oka S, Samukawa K, Azuma I. Inhibitory effect of tumor metastasis in mice by saponins, ginsenoside-Rb2, 20(R)- and 20(S)-ginsenoside-Rg3, of red ginseng. Biol Pharm Bull 1995;18:1197-1202.

  113. Byun BH, Shin I, Yoon YS, Kim SI, Joe CO. Modulation of protein kinase C activity in NIH 3T3 cells by plant glycosides from Panax ginseng. Planta Med 1997;63:389-392.

  114. Surh YJ, Na HK, Lee JY, Keum YS. Molecular mechanisms underlying anti-tumor promoting activities of heat-processed Panax ginseng C.A. Meyer. J Korean Med Sci 2001;16:38-41.

  115. Keum YS, Park KK, Lee JM, Chun KS, Park JH, Lee SK, Kwon H, Surh YJ. Antioxidant and anti-tumor promoting activities of the methanol extract of heat-processed ginseng. Cancer Lett 2000;150:41-48.

  116. Subbaramaiah K, Telang N, Ramonetti JT, Araki R, DeVito B, Weksler BB, Dannenberg AJ. Transcription of cyclooxygenase-2 is enhanced in transformed mammary epithelial cells. Cancer Res 1996;6:4424-4429.

  117. O’Brien  TG. The induction of ornithine decarboxylase as an early, possibly obligatory event in mouse skin carcinogenesis. Cancer Res 1976;36:2644-2653.

  118. Mayo MW, Wang CY, Congswell PC, Rogers-Graham KS, Lowe SW, Der CJ, Baldwin AS. Requirement of NF-κB activation to suppress p53-independent apoptosis induced by oncogenic Ras. Science 1997;278:1812-1915.

  119. Murphy LL, Cadena RS, Chavez D, Ferraro JS. Effect of American ginseng (Panax quinquefolium) on male copulatory behaviour in the rat. Physiology & Behavior 1998;64:445-450.

  120. Kim C, Choi H, Kim CC, Kim JK, Kim MS, Ahn BT, Park HJ. Influence of ginseng on mating behaviour of male rats. Am J Chin Med 1976;4:163-168.

  121. Choi HK, Seong DH, Rha KH. Clinical efficacy of Korean red ginseng for erectile dysfunction. Int J Impot Res 1995;7:181-186.

  122. Chen X, Lee TJ. Ginsenosides-induced a nitric oxide-mediated relaxation of the rabbit corpus cavernosum. Br. J. Pharmacol 1995;115:15-18.

  123. Fahim MS, Fahim Z, Harman JM. Effect of Panax ginseng on testosterone level and prostate in male rats. Arch Androl 1982;8:261-263.

  124. Bahrke MS, WP Morgan. Evaluation of the ergogenic properties of ginseng. Sports Med 1994;18:229-248.

  125. Suzuki Y, Hikino H. Mechanisms of hypoglycaemic activity of panaxans A and B, glycans of Panax ginseng roots: effects on plasma level, secretion, sensitivity and binding of insulin in mice. Phytother Res 1989;3:20-24.

  126. Ng TB, Yeung HW. Hypoglycemic constituents of Panax ginseng. Gen Pharmacol 1985;16:549-552.

  127. Tchilian EZ, Zhelezarov IE, Hadjiivanova CI. Effect of ginsenoside Rg1 on insulin binding in mice liver and membranes. Phytother Res 1991;5:46-48.

  128. Wang LC, Lee TF. Effect of ginseng saponins on cold tolerance in young and elderly rats. Planta Med 2000;66:144-147.

  129. Park DL. Effect of Panax ginseng on x-ray irradiation and synergetic study on nitromin. Insam Munhun Teukjip 1964;2:55-65.

  130. Pande S, Dumar M, Kumar A. Evaluation of radimodyfing effect of root extract of Panax ginseng. Phytother Res 1998;12:13-17.

  131. Yonezawa M, Takeda A, katoh N. Restoration of radiation injury by ginseng extract. Proceeding of the Third International Ginseng Symposium, Soul, Republic of Korea 1980: 17-20.

  132. Kim C, Choi JE. Effect of radioprotective ginseng protein on UV-induced sister chromatid exchanges. Arch Pharm Res 1988;11:93-98.

  133. Wang B, Cui J, Liu A. Effect of saponins isolated from stems and leaves of ginseng (SSLG) on experimental liver injury. Acta Pharm Sinica 1983;18:726-731.

  134. Hikino H, Kiso Y, Kinouchi J, Sanada S, Shoji J. Validity of the oriental medicines. 73 liver-protective drugs. 18 antihepatotoxic actions of ginsenosides from Panax ginseng roots. Planta Med 1985;1:62-64.

  135. Wang BX, Cui JC, Liu AJ. The effect of ginseng on immune responses. Advances in Chinese Medicinal Material Research 1985:519-527.

  136. Chang PH. The effect of ginseng (Panax ginseng C.A. Meyer) on organism activity. Acta Pharm Sinica 1966;13:106-111.

  137. Jeong CS, Hyun JE, Kim YS. Ginsenoside Rb1: the anti-ulcer constituent from the head of Panax ginseng. Arch Pharm Res 2003;26:906-911.

  138. Wang BX, Cui JC, Liu AJ. The action of ginsenosides extracted from the stems and leaves of Panax ginseng in promoting animal growth. Yao Xue Xue Bao 1982;17:899-904.

  139. Hess FG, Parent RA, Stevens KR, Cox GE, Becci PJ. Effects of aubchronic feeding of ginseng extract G115 in beagle dogs. Food Chem Toxicol 1983;21: 95-97.

  140. Coon JT, Ernst E. Panax ginseng: a systematic review of adverse effects and drug interactions. Drug Saf 2002;25:323-344.

  141. Siegel RK. Ginseng abuse syndrome-problems with the panacea. JAMA 1979;241:1614-1615.

Copyright © 2004 by Razi Institute for Drug Research (RIDR)

The following images related to this document are available:

Photo images

[pt04005f3.jpg] [pt04005f4.jpg] [pt04005f2.jpg] [pt04005f1.jpg]
Home Faq Resources Email Bioline
© Bioline International, 1989 - 2014, Site last up-dated on 14-Apr-2014.
Site created and maintained by the Reference Center on Environmental Information, CRIA, Brazil
System hosted by the Internet Data Center of Rede Nacional de Ensino e Pesquisa, RNP, Brazil