Effect of Panax ginseng extract on tissue glycogen and adrenal
cholesterol depletion during prolonged exercise
The acute effect of Panax ginseng (GS), root extract was investigated on the rate of glycogenolysis in white muscle and in
liver during prolonged exercise of 3 hours duration in rats. Adrenal cholesterol depletion was also measured. GS inhibited
decrease of adrenal cholesterol by 21% after 3 hours of swimming. GS had no effect on hepatic glycogen, but had pronounced
inhibitory effects on endogenous glycogen utilization in white skeletal muscle during exercise. These findings indicate that
GS has carbohydrate-sparing actions during prolonged exercise, and suggests a possible physiological basis for ginseng’s
anti-fatigue properties. Avakian EV Jr, Evonuk E. Planta Med 1979 May;36(1):43-48.
Effect of Panax ginseng extract on energy metabolism during exercise in rats
We examined the acute effects if ginseng extract (GS) administration on arterial plasma levels of glucose, free fatty acids
(FFA), lactic acid (LA) and pyruvic acid (PA) in resting rats, and in animals that swam for 30 or 60 minutes. Compared to
vehicle-treated (saline) control animals, GS did not significantly alter these parameters at rest. During exercise, GS-treated
animals had higher blood glucose levels than control rats, and markedly lower concentrations of circulating LA and PA.
Plasma FFA was also lower in the GS-treated animals at 30 minutes of swimming. These results provide evidence that
ginsengosides can significantly alter mechanisms of fuel homeostasis during prolonged exercise, presumably by increasing
the biochemical capacity of skeletal muscle to oxidize FFA in preference for cellular energy production. Avakian EV, Sugimoto
RB, Taguchi S, Horvath SM. Planta Med 1984 Apr;50(2):151-154.
In vitro effects of echinacea and ginseng on natural killer and
antibody-dependent cell cytotoxicity in healthy subjects and
chronic fatigue syndrome or acquired immunodeficiency
Extracts of Echinacea purpurea and Panax ginseng were evaluated for their capacity to stimulate cellular immune function
by peripheral blood mononuclear cells (PBMC) from normal individuals and patients with either the chronic fatigue syndrome
or the acquired immunodeficiency syndrome. PBMC isolated on a Ficoll-hypaque density gradient were tested in the presence
or absence of varying concentrations of each extract for natural killer (NK) cell activity versus K562 cells and antibody-
dependent cellular cytotoxicity (ADCC) against human herpesvirus 6 infected H9 cells. Both echinacea and ginseng, at
concentrations > or = 0.1 or 10 micrograms/kg, respectively, significantly enhanced NK-function of all groups. Similarly, the
addition of either herb significantly increased ADCC of PBMC from all subject groups. Thus, extracts of Echinacea purpurea
and Panax ginseng enhance cellular immune function of PBMC both from normal individuals and patients with depressed
cellular immunity. See DM, Broumand N, Sahl L, Tilles JG. Immunopharmacology 1997 Jan;35(3):229-235.
Antistress and antifatigue properties of Panax ginseng:
comparison with piracetam
The antistress and antifatigue properties of a Chinese ginseng preparation were tested on Swiss albino mice, exposed to
various experimental models of stress, and were compared with those of piracetam. Both ginseng and piracetam were
administered chronically in drinking water for 16-18 days as well as acutely, by injection, 30-60 min prior to the experiments.
Reactivity of the mice, loss in body weight, amount of faeces, length of endurance and incidence of mortality were graded
and measured. Both piracetam and ginseng treatment provided good protection against electroshock stress when compared
to the untreated mice; fighting scores, incidence of tonic convulsion and mortality were significantly less in the treated
groups. In the heat stress experiments, both piracetam and ginseng provided significant protection to the treated mice
against exposure to heat. In the fatigue stress of forced swim test, ginseng treatment provided effective adaptation to fatigue
and increased endurance in both male and female mice; piracetam showed some antifatigue effects on the male mice only.
In the locomotor activity tests, ginseng did not depress motility, while piracetam did so in the later part of the tests. Banerjee
U, Izquierdo JA. Acta Physiol Lat Am 1982;32(4):277-85.
Anti-proliferating effects of ginsenoside Rh2 on MCF-7 human
breast cancer cells
Ginsenoside Rh2 (G-Rh2) isolated from the root of Panax ginseng has been shown to have anti-cancer proliferation,
differentiation and chemopreventive effects in certain cancer cell types. We investigated the mechanism of G-Rh2-induced
growth inhibition in MCF-7 human breast carcinoma cells. G-Rh2 significantly inhibited the cell growth in a concentration-
dependent manner, which effect was reversible, and induced a G1 arrest in cell cycle progression. G-Rh2 treatment down-
regulated the protein level of cyclin D3 but upregulated the expression of cyclin-dependent kinase (Cdk) inhibitor p21WAF1/
CIP1. The increased levels of p21 were associated with increased binding of p21 and Cdk2 concomitant with marked decrease
in Cdk2 and cyclin E-dependent kinase activities with no changes in Cdk2 and cyclin E expression. G-Rh2 markedly reduced
the phosphorylated retinoblastoma protein (pRb) and enchanced association of unphosphorylated pRb and the transcription
factor E2F-1. These data suggest that G-Rh2 inhibited the growth of MCF-7 cells, by inducing protein expression of p21 and
reducing the protein levels of cyclin D which resulted in the down-regulation of cyclin/Cdk complex kinase activity, decreasing
phosphorylation of pRb, and inhibiting E2F release. Oh M, Choi YH, Choi S, Chung H, Kim K, Kim SI, Kim DK, Kim ND. Int
J Oncol 1999 May;14(5):869-75.
Non-organ specific cancer prevention of ginseng: a prospective
study in Korea
BACKGROUND: A number of studies have reported that increased consumption of natural products reduced the risk of
cancer. Our previous case-control studies have shown a significant reduction in the risk of cancer development among those
who regularly consumed ginseng. We conducted a prospective cohort study to evaluate the preventive effect of ginseng
against cancer on a population residing in a ginseng cultivation area on the basis of the result of case-control studies.
METHODS: This study was conducted in Kangwha-eup from August 1987 to December 1992. We studied 4634 people over
40 years old who completed a questionnaire on ginseng intake. In an attempt to obtain detailed information about ginseng
intake, we asked them to specify their age at initial intake, their frequency and duration of ginseng intake, the kind of ginseng,
etc. Multiple logistic regression was used to estimate relative risks (RR) when controlling simultaneously for covariates.
RESULTS: Ginseng consumers had a decreased risk (RR = 0.40, 95% confidence interval [CI] : 0.28-0.56) compared with
non-consumers. On the type of ginseng, the RR was 0.31 (95% CI: 0.13-0.74) for fresh ginseng extract consumers and 0.34
(95% CI: 0.20-0.53) for consumers of multiple combinations. There was no cancer death among 24 red ginseng consumers.
There was a decreased risk with a rise in the frequency of ginseng intake, showing a dose-response relationship. The RR of
ginseng consumers were 0.33 (95% CI: 0.18-0.57) in gastric cancer and 0.30 (95% CI : 0.14-0.65) in lung cancer. Among
ginseng preparations, fresh ginseng extract consumers were significantly associated with a decreased risk of gastric cancer
(RR = 0.33, 95% CI: 0.12-0.88). CONCLUSIONS: These results strongly suggest that Panax ginseng C.A. Meyer has non-
organ specific preventive effect against cancer, providing support for the previous case-control studies. Yun TK, Choi SY.
Int J Epidemiol 1998 Jun;27(3):359-64.
Ginsenoside-induced relaxation of human bronchial smooth muscle via release of nitric
Ginsenoside, an extract of Panax ginseng, is an essential constituent of anti-asthmatic Chinese herbal medicine. To eluci-
date whether ginsenoside affects airway smooth muscle tone and, if so, what the mechanism of action is, we studied relaxant
responses of human bronchial strips under isometric condition in vitro, and directly measured the release of nitric oxide (NO)
by an amperometric sensor for this molecule. Addition of ginsenoside relaxed the tissues precontracted with acetylcholine in
a dose-dependent manner, the maximal relaxation and the ginsenoside concentration required to produce 50% relaxation
being 67+/-8% and 210+/-29 microg ml(-1), respectively. The relaxant responses to ginsenoside were inhibited by N(G)-
nitro-L-arginine methylester (L-NAME) and removal of the epithelium, but not by N(G)-nitro-D-arginine methylester (D-NAME)
or tetrodotoxin. This inhibitory effect of L-NAME was reversed by L-arginine but not by D-arginine. Addition of ginsenoside to
the medium containing bronchial tissues dose-dependently increased NO-selective electrical current, and this effect was
greatly attenuated by the epithelial removal or Ca(2+)-free medium. Ginsenoside also increased tissue cyclic GMP contents,
an effect that was abolished in the presence of L-NAME. It is concluded that ginsenoside induces relaxation of human
bronchial smooth muscle via stimulation of NO generation predominantly from airway epithelium and cyclic GMP synthesis.
This action might account for the anti-asthmatic effect of Panax ginseng. Tamaoki J, Nakata J, Kawatani K, Tagaya E, Nagai
A. Br J Pharmacol. 2000 Aug;130(8):1859-64.
Effects of ginsenosides from Panax ginseng on cell-to-cell communication function
mediated by gap junctions
Gap junctions have been shown or are believed to be involved in the pathogenesis of many inherited and acquired human
diseases. Agents that regulate the gap junction-mediated intercellular communication (GJIC) function may facilitate preven-
tion and treatment of GJIC-involved diseases. In the present study we examined the effects of 27 ginsenosides isolated from
Panax ginseng on GJIC. The results show that compounds 1 (oleanolic acid), 2 (ginsenoside-R0), 3 (ginsenoside-Rb1), 5
(ginsenoside-Rb2), 7 (ginsenoside-Rd), 8 (ginsenoside-Rg3), 12 (panaxadial), 13 (notoginsenoside-R4), 17 [ginsenoside-
Rg2 (20S)], 18 (ginsenoside-Rf), and 26 (ginsenoside-F3) did not obviously affect GJIC, whereas compounds 4 (ginsenoside-
Rc), 6 (ginsenoside-Rb3), 9 (ginsenoside-Rd2), 10 (notoginsenoside-Fe), 11 (ginsenoside-Rh2),14 (ginsenoside-Ra1), 15
(ginsenoside-Re), 16 [ginsenoside-Rg2 (20R)], 19 (ginsenoside-Ia), 20 [ginsenoside-Rh1 (20S)], 21 [ginsenoside-Rh1 (20R)],
22 (ginsenoside-F1), 23 (protopanaxatriol), 24 (panaxatriol), 25 (ginsenoside-Rg1), and 27 (chikusetsaponin-L8) induced
GJIC reductions at various degrees. Compounds 2, 7, and 8 protected against the tyrosine phosphatase inhibitor vanadate-
induced GJIC reduction, while compounds 1, 5, 7, and 17 inhibited the cytokine interleukin 1 alpha (IL-1alpha)-induced
reduction in GJIC. Nevertheless, no compounds protected against the protein kinase C (PKC) activator 12-O-
tetradecanoylphorbol-13-acetate (TPA)-induced GJIC inhibition. On the other hand, GJIC reductions induced by compounds
6, 9,10, 20, 21, 22, 24, and 25 were inhibited by the tyrosine kinase (TK) inhibitor genistein, while GJIC reductions induced
by compounds 6, 9, 14, 16, 19, 21, and 24 were attenuated in the presence of the PKC inhibitor calphostin C. However, GJIC
reductions induced by compounds 4, 23, and 27 were not inhibited either by genistein or by calphostin C. These data indicate
that various mechanisms are responsible for effects of ginsenosides on GJIC. Zhang YW, Dou DQ, Zhang L, Chen YJ, Yao
Extracts of Ginkgo biloba and Panax ginseng protect brain proteins from free radical
induced oxidative damage in vitro
Oxidative damage to normal human brain tissue was induced following exposure to hydroxyl (OH.) or superoxide (O2-.) free
radical species generated by CO60 irradiation in vitro. Both enzymic and cytoskeletal proteins showed substantial (dose
dependent) oxidative damage following exposure to OH. or O2-., as quantified by SDS-polyacrylamide gel electrophoretic
analysis. Extracts of Ginkgo biloba or Panax ginseng showed a remarkable capacity to protect brain tissue proteins from
oxidative damage in vitro, even at extreme (2000 kRads) dosage levels of OH. or O2-.. We suggest, therefore, that the
beneficial effect of these plant extracts in preventing brain tissue damage in vivo (e.g. following ischemia-reperfusion) may
result from their action in protecting brain proteins from oxidative damage, in addition to their previously reported capacity to
reduce free radical induced lipid peroxidation. Siddique MS, Eddeb F, Mantle D, Mendelow AD. Acta Neurochir Suppl
The preceding abstracts were obtained from the Medline service maintained by the National Institutes of Health.