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Curcumin, demethoxycurcumin and bisdemethoxycurcumin have antioxidant activity. They may also posses anticarcinogenic, anti-inflammatory, antiviral and hypocholesterolemic activities. The curcuminoids have been found to have a number of antioxidant activities, including scavenging of such reactive oxygen species as superoxide anions and hydrogen peroxide, inhibition of lipid peroxidation and inhibition of the oxidation of low-density lipoprotein (LDL). The reduced derivative of curcumin, tetrahydrocurcumin, has been found to have even stronger antioxidant activity. Tetrahydrocurcumin may be formed from curcumin following ingestion; but this is unclear. The possible anticarcinogenic activity of curcumin and the other curcuminoids may be accounted for by a few mechanisms. These include inhibition of angiogenesis, upregulation of apoptosis, interference with certain signal transduction pathways that are critical for cell growth and proliferation, inhibition of colonic mucosa cyclooxygenase (COX) and lipoxygenase (LOX) activities and inhibition of farnesyl protein transferase. In addition to its possible activity in preventing malignant transformation and inhibiting tumor growth, curcumin may have antimetastatic potential, as well. In this regard, curcumin has been found to inhibit matrix metalloproteinase-9 in a human hepatocellular carcinoma cell line. The possible anticarcinogenic activity of the curcuminoids may be attributed, at least in part, to their ability to inhibit activation of the transcription factors NF-KappaB and AP-1. Curcuminoids have also been found to target the fibroblast growth factor-2 (FGF-2) angiogenic signaling pathway and inhibit expression of gelatinase B in the angiogenic process. In the final analysis, the curcuminoids' antioxidant activity may underlie many of the above mechanisms. Reactive oxygen species (ROS) can activate AP-1 and NF-KappaB. Further, FGF-2 induces AP-1 activation via ROS produced through NADPH oxidase. The curcuminoids, acting as antioxidants, may interfere with the ability of FGF-2 to stimulate AP-1, and they may generally inhibit the activation of NF-KappaB and AP-1. The possible anti-inflammatory activity of the curcuminoids may also be accounted for by several mechanisms, including inhibition of COX and LOX, reduction of the release of ROS by stimulated neutrophils, inhibition of AP-1 and NF-KappaB, and inhibition of the activation of the pro-inflammatory cytokines TNF (tumor necrosis factor) -alpha and IL (interleukin)-1 beta. Curcumin has modest anti HIV-1 activity. It has been found to inhibit HIV-1 and HIV-2 proteases, HIV-1 LTR (long terminal repeat)-directed gene expression, Tat-mediated transactivation of HIV-1-LTR and HIV-1 integrase. All of these actions have been demonstrated in vitro. There is no evidence that curcumin or the other curcuminoids significantly inhibit the replication of HIV-1 in vivo. The mechanism of the possible hypocholesterolemic effect of the curcuminoids is unclear. The pharmacokinetics of the curcuminoids remain only partly understood. Of the curcuminoids, curcumin has been most studied, mainly in animals. Curcumin is poorly absorbed following ingestion in mice and rats. In these animals, 38 to 75% of an ingested dose is excreted directly in the feces. Absorption appears to be better with food. In mice, the major metabolites of curcumin are curcumin glucuronoside, dihydrocurcumin glucuronoside, tetrahydrocurcumin glucuronoside and tetrahydrocurcumin. These metabolites are formed in the liver. Animal studies and the pharmacokinetics of curcumin are continuing. Human pharmacokinetic studies are needed.
The rhizomes contain curcuminoids, curcumin, demethoxy curcumin, bis- demethoxycurcumin, 5'- methoxycurcumin and dihydrocurcumin which are found to be natural anti-oxidants. A new curcuminoid, cyclocurcumin, was isolated from the nematocidally active fraction of turmeric. The fresh rhizomes also contain two nnatural phenolics which possess antioxidant and anti-inflammatory activities and also two new pigments. Several sesquiterpenes, germacrone, turmerone, ar-(+)-, a-, ß- turmerones; ß- bisabolene; a-curcumene; zingiberene; ß- sesquiphellandene, bisacurone; curcumenone; dehydrocurdione; procurcumadiol; bis-acumol; curcumenol; isoprocurcumenol epiprocurcumenol; procurcumenol; zedoaronediol; curlone; and turmeronol A and turmeronol B, have been recorded from the rhizomes. The rhizomes also contain four polysaccharides-ukonans - having activity on the Reticuloendothelial system, along with stigmasterol, ß-sitosterol, cholesterol and 2-hydroxymethyl anthraquinone
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Curcumin blocks cytokine-mediated NF-kappa B activation and proinflammatory gene expression by inhibiting inhibitory factor I-kappa B kinase activity. J Immunol 163:3474-83. Kawamori T, et al. 1999. Chemopreventive effect of curcumin, a naturally occurring anti-inflammatory agent, during the promotion/progression stages of colon cancer. Cancer Res 59:597-601. Korutla L, et al. 1995. Inhibition of ligand-induced activation of epidermal growth factor receptor tyrosine phosphorylation by curcumin. Carcinogenesis 16:1741-5. Lertratanangkoon K, et al. 1997. Increase of unmethylated CpG sites in genomic DNA by glutathione-depleting agent (Meeting abstract). Proc Annu Meet Am Assoc Cancer Res 38:A1205. Lertratanangkoon K, et al. 1999. Inhibition of glutathione synthesis with proppargylglycine enhances N-acetylmethionine protection and methylation in bromobenzene-treated Syrian hamsters. J Nutr 129:649-56. Lin LI, et al. 1998. 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