If you are diabetic it is ill advised. Ginseng has a remarkable affect on the adrenal glands and this may impact on sugar regulation. Always consult your doctor before using Ginseng.
Ginseng is known to interfere with the actions of various pharmaceutical drugs.
Ginseng should not be used on a continual basis, it can induce adrenal exhaustion.
Article: Inflammation, Cancer, and Targets of Ginseng
Image:
Authors: Lorne J. Hofseth and Michael J. Wargovich
Journal: J. Nutr. 137: 183S–185S, 2007.
Location: Life\Nutrition\Title
Date obtained: 18/10/2008
Date Read: 21/10/2008
Date to Review:
Web Page:
Keywords:
Printed:
Notes:
Abstract
Chronic inflammation is associated with a high cancer risk. At the molecular level, free radicals and aldehydes, produced during chronic inflammation, can induce deleterious gene mutation and posttranslational modifications of key cancerrelated proteins. Other products of inflammation, including cytokines, growth factors, and transcription factors such as nuclear factor kB, control the expression of cancer genes (e.g., suppressor genes and oncogenes) and key inflammatory enzymes such as inducible nitric oxide synthase and cyclooxygenase-2. These enzymes in turn directly influence reactive oxygen species and eicosanoid levels. The procancerous outcome of chronic inflammation is increased DNA damage, increased DNA synthesis, cellular proliferation, disruption of DNA repair pathways and cellular milieu, inhibition of apoptosis, and promotion of angiogenesis and invasion. Chronic inflammation is also associated with immunosuppression, which is a risk factor for cancer. Current treatment strategies for reactive species overload diseases are frequently aimed at treating or preventing the cause of inflammation. Although these strategies have led to some progress in combating reactive species overload diseases and associated cancers, exposure often occurs again after eradication, treatment to eradicate the cause fails, or the treatment has long-term side effects. Therefore, the identification of molecules and pathways involved in chronic inflammation and cancer is critical to the design of agents that may help in preventing the progression of reactive species overload disease and cancer associated with disease progression. Here, we use ginseng as an example of an antiinflammatory molecule that targets many of the key players in the inflammation-to-cancer sequence. J. Nutr. 137: 183S–185S, 2007.
TABLE 1 Key players in the inflammation-to-cancer sequence1
The inflammatory player: Examples of mechanisms toward carcinogenesis
RONS, COX, and NOS Damage DNA, modify cancer protein, alter proliferation and
apoptosis (depending on concentration, microenvironment, and genetic background
of target cells), inactivate tumor suppressor pathways (e.g., pRb and p53).
NF-kB Activate proliferation and inhibit apoptosis by activating modulators of these
event: cytokines (e.g., TNF-a), growth factors, survival genes (e.g., Bcl-XL),
angiogenic factors (e.g., VEGF), inflammatory genes (e.g., COX and NOS). Recent
high profile studies indicate this molecule is a key molecular node in the
inflammation-to-cancer sequence (2).
TLRs Activate MAP kinase and NF-kB pathways.
Cytokines Activate or deactive many inflammation and cancer pathways (1). Example:
The proinflammatory cytokine, IL-6 can antagonize p53, inactivate pRb, and activate
survival genes (Bcl-2 and Bcl-XL); The antiinflammatory cytokine, IL-10, can inhibit
proliferation and ras signaling.
Growth factors Transforming growth factor-b, at high concentrations, activates
p21/p27-mediated growth arrest and smad- and p53-mediated apoptosis.
MMPs MMP-2 promotes proliferation by activation of the discoidin domain tyrosine
kinase receptor 2. MMPs also are immunomodulators and stimulate angiogenesis,
inhibit cell adhesion, and inhibit apoptosis.
PPARs PPAR-g ligands are mostly protective to the inflammation- to-cancer sequence.
They inhibit iNOS, COX-2, NF-kB, MMPs, and E2Fs; they activate p53, p27, and p21.
Kinase pathways p38 stimulates proliferation and inhibits apoptosis. An inhibitor of
MAP kinase signaling (CNI-1493) has shown promise in ameliorating Crohn disease
in humans (3).
p53 and pRb pathways Both pathways are inactivated in reactive species overload
diseases (4,5).
Studies indicate that ginseng has potential as a chemopreventive agent or adjuvant treatment. Some of the cancers shown to decrease significantly with ginseng use include cancersof the pharynx, stomach, liver, pancreas, and colon (22,23). Mechanisms include inhibition of DNA damage (24), induction of apoptosis (25), and inhibition of cell proliferation (26). It is also becoming increasingly clear that ginseng has potent effects on the inflammatory cascade and may inhibit the inflammationto- cancer sequence.
--
Ginseng targets the inflammatory players There is evidence that ginseng has potent effects on key players in the inflammatory cascade (Fig. 1). For example, ginsan, a polysaccharide extracted from P. ginseng, showed inhibition of s, the p38 MAP kinase pathway, and NF-kB in vitro and inhibition of proinflammatory cytokines in vivo (27). The ginsenoside Rg3 was shown to inhibit phorbol ester–induced COX-2 and NF-kB induction (28). BST204, a fermented ginseng extract, can inhibit inducible NOS (iNOS) expression and subsequent nitric oxide production from lipopolysaccharidestimulated RAW264.7 murine macrophages.
--
Ginseng can also inhibit other mediators of the inflammation- to-cancer sequence, such as matrix metalloproteases and kinase pathways (31).
--
Project:
