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Oral intake of standardised P. ginseng extract demonstrates a dose dependant (1, 3 or 10 mg/kg) chemoprotective and antimutagenic effect in animal studies (Panwar et al 2005) and ginsenoside Rg3 has recently been produced as an antiangiogenic anticarcinogenic drug in China (Shibata 2001 ).

Chemoprotection Oral administration of red ginseng extracts (1% in diet for 40 weeks) significantly (P < 0.05) suppressed spontaneous liver tumour formation in male mice. Oral white ginseng was also shown to suppress tumour promotion in vitro and in vivo (Nishino et al 2001 ).

Dietary administration of red ginseng in combination with 1,2-dimethylhydrazine suppresses colon carcinogenesis in rats (rats were fed 1% ginseng for 5 weeks). It is thought that the inhibition may be partly associated with inhibition of cell proliferation in the colonic mucosa (Fukushima et al 2001).

Oral administration of 50 mg/kg/day for 4 weeks of a ginseng intestinal metabolite has been shown to partially protect against doxorubicin-induced testicular toxicity in mice. The metabolite significantly (P < 0.01 ) prevented decreases in body weight, spermatogenic activities, serum levels of lactate dehydrogenase and creatine phosphokinase induced by doxorubicin. It also significantly attenuated germ cell injuries (Kang et al 2002).

The methanol extract of red ginseng has been shown to attenuate the lipid peroxidation in rat brain and scavenge superoxides in differentiated human promyelocytic leukaemia (HL-60) cells. Topical application of the same extract, as well as purified ginsenoside Rg3, has been demonstrated to suppress skin tumour > 2007 Elsevier Australia

promotion in mice. Rg3 also suppresses COX, NF-kappa B and extracellular-regulated protein kinase, which are all involved in tumour promotion (Surh et al 2001 ).

Pretreatment with oral red ginseng extract significantly reduced the development of cancer from diethylnitrosamine-induced liver cancer nodules in rats (the developmental rate of liver cancer in the experimental group was 14.3% compared with 100% in the control group). When ginseng was given concomitantly with diethylnitrosamine, the hepatoma nodules were smaller than those of the control group, the structure of hepatic tissue was well preserved and the structure of hepatocytes was normal. Ginseng also prolonged the average life span. These findings suggest benefits of ginseng in the prevention and treatment of liver cancer (Wu et al 2001).

Irradiation protection Ginsenosides and specifically panaxadiol have been shown to have radioprotective effects in mice irradiated with high-dose and low-dose gamma radiation. Jejunal crypts were protected by pretreatment with extract of whole ginseng (50 mg/kg body weight intraperitoneally at 12 and 36 hours before irradiation, P < 0.005). Extract of whole ginseng (P < 0.005), total saponin (P < 0.01) or panaxadiol (P < 0.05) administration before irradiation (50 mg/kg body weight IP at 12 and 36 hours before irradiation) resulted in an increase in the formation of the endogenous spleen colony. The frequency of radiation-induced apoptosis in the intestinal crypt cells was also reduced by pretreatment with extract of whole ginseng, total saponin and panaxadiol (Kim et al 2003).

These radioprotective effects are partly associated with the immunomodulatory effect of ginseng. Ginsan, a purified polysaccharide isolated from ginseng, has been shown to have a mitogenic activity, induce lymphokine-activated killer cells and increase levels of several cytokines. Ginsan reduced mutagenicity in a dose-dependent manner when applied to rats 30 min before or 1 5 min after 1.5 Gy of gammairradiation. The radioprotective effect of ginsan has been partly attributed to a reduction in radiation-induced genotoxicity (Ivanova et al 2005). Ginsan has also been found to increase the number of bone marrow cells, spleen cells, granulocyte-macrophage colony-forming cells and circulating neutrophils, lymphocytes and platelets significantly in irradiated mice (Song et al 2003).

One of the causes of radiation damage is lipid peroxidation, which alters lysosomal membrane permeability leading to the release of hydrolytic enzymes. Ginseng has been shown to markedly inhibit lipid peroxidation and protect against radiation damage in testes of mice (Kumar et al 2003). Antitumour, antiproliferative, antimetastatic and apoptosis-inducing Stimulation of the phagocytic activity of macrophages may play a role in

the anticarcinogenic and antimetastasic activities demonstrated for ginseng in vivo (Shin et al 2004b) and research has continually found tumour inhibitory effects, especially in the promotion and progression phases (Helms 2004).

Ginsenosides Rg3, Rg5, Rk1, Rs5 and Rs4 have been shown to be cytotoxic to Hep-1 hepatoma cancer cells in vitro. Their 50% growth inhibition concentration (GI50) values were 41, 11, 13, 37, and 13 micromol/L respectively. Cisplatin had a GI50 of 84 micromol/L in the same assay conditions (Park et al 2002a).

Constituents in ginseng have also been shown to inhibit proliferation of cancer cells. Panaxytriol isolated from red ginseng was shown to have significant dose-dependent cytotoxicity activity and inhibit DNA synthesis in various tumour cells tested (Kim et al 2002a). Ginsenoside Rg3 has displayed inhibitory activity against human prostate cancer cells in vitro (Liu et al 2000).

Ginsenosides, especially 20(R)-ginsenoside Rg3, has been shown to specifically inhibit cancer cell invasion and metastasis (Shibata 2001 ) and ginsenoside Rh2 has been shown to inhibit human ovarian cancer growth in mice (Nakata et al 1998). It is likely that the anti-tumour promoting activity of Rg3 is mediated through down-regulation of NF-kappa B and other transcription factors (Keum et al 2003).

Oral administration of 20(S)-protopanaxatriol (M4), the main bacterial metabolite of protopanaxatriol-type ginsenosides, has been shown to inhibit melanoma growth in mice and pretreatment was shown to reduce metastases to the lungs. This effect is thought to be due to stimulation of NK-mediated tumour lysis (Hasegawa et al 2002)

The antimetastatic effects of ginseng are related to inhibition of the adhesion and invasion of tumour cells and also to antiangiogenesis activity. Ginsenosides Rg3 and Rb2 have been shown to significantly inhibit adhesion of melanoma cells to fibronectin and laminin, as well as preventing invasion into the basement membrane in vitro. Other experiments have demonstrated that the saponins exert significant antiapoptotic activity, decreasing the number of blood vessels oriented toward the tumour mass (Mochizuki et al 1995, Sato et al 1994).

Ginseng saponins have also been found to promote apoptosis (programmed cell death) in cancer cells in vitro (Hwang et al 2002).

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