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Curcumin and Oral Carcinoma Cells
Molecular Mechanisms of Anti-angiogenic Effect of Curcumin Curcumin Suppresses Activation of NF-kappaB and AP-1 Novel Approaches for Colon Cancer Prevention Chemopreventive Efficacy and Pharmacokinetics of Curcumin The Chemopreventive Compound Curcumin Curcumin and Human Prostate Cancer Cells Phase I Clinical Trial of Curcumin Curcumin and Gastrointestinal Cancers Curcumin 95% ( reconstituted bio-enhanced turmeric extract) Below are excerpts from The Churchill Livingstone publication titled “Text Book of Natural Medicine” by Joseph E Pizzorno Jr (President and Faculty, Bastyr University, Kenmore, Washington, USA) and Michael T Murray ND (Faculty, Bastyr University, Kenmore, Washington, USA), 1999 Edition. Curcuma longa (turmeric) pages 689-693 Turmeric is a perennial herb of the ginger family, extensively cultivated in India, China, Indonesia, and other tropical countries. Chemical composition: Turmeric contains: 4 – 14% of an orange-yellow volatile oil that is composed mainly of turmerone, atlantone, and zingiberone. 0.3 – 5.4% curcumin sugars (28%glucose, 12%fructose, 1% arabinose) resins protein vitamins minerals History & folk use: Turmeric is the major ingredient of curry powder and is also used in prepared mustard. It is extensively used in foods for both its colour and flavor. In addition, turmeric is used in both the Chinese and Indian (Ayurvedic) system of medicine as an anti-inflammatory agent and in the treatment of numerous conditions, including flatulence, jaundice, menstrual difficulties, bloody-urine, hemorrhage, toothache, bruises, chest pain, and colic. Turmeric poultices are often applied locally to relieve inflammation and pain. Pharmacology: Turmeric and its derivatives have a great deal of pharmacological activity. Although a number of components have demonstrated activity, the volatile oil components and curcumin are believed to be the most active components. Turmeric has been found to be: an effective antioxidant anticarcinogenic anti-inflammatory cardiovascular hepatic gastro-intestinal an anti-microbial agent Antioxidant activity is comparable to standard antioxidants like Vitamin C and E and BHA and BHT. Anticarcinogenic effects have been demonstrated at all steps of carcinogenesis: initiation, promotion and progression. In addition to inhibiting the development of cancer, several studies have suggested that curcumin can also promote cancer regression. Turmeric and curcumin are non-mutagenic and have been shown to suppress themutagenicity of several common mutagens (cigarette smoke condensates, benzopyrene, DMBA, etc.) as do chili and capsaicin. Turmeric and curcumin have also demonstrated impressive anti-cancer effects against a number of chemical carcinogens on a wide range of cell types in both in vitro and in vivo studies. Curcumin has demonstrated an impressive ability to reduce the levels of urinary mutagens. The protective effects of of turmeric and its derivatives are only partially explained by by its direct antioxidant and free radical scavenging effects. It also inhibits nitrosamine formation, enhances the body’s natural antioxidant system, increases the levels of glutathione and other non-protein sulfhydryls, and acts directly on several enzymes and gene loci. Anti-inflammatory effects of the oil fraction of curcuma longa has been demonstrated in a variety of experimental models, e.g.Freund’s adjuvant-induced arthritis, formaldehyde and carrageenan-induced paw edema, and cotton pellet and granuloma pouch tests. Its effects in these studies were comparable to cortisone and phenylbutazone. Even more potent in acute inflammation is curcumin. Curcumin is as effective as cortisone or phenylbutazone in models of acute inflammation, but only half as effective in chronic models. However, while phenylbutazone and cortisone are associated with significant toxicity, curcumin displays virtually no toxicity. Curcumin’s counter-irritant effect may also be a major factor in its topical anti-inflammatory action. Used orally, curcumin exhibits many direct anti-inflammatory effects including: inhibition of leukotriene formation inhibition of platelet aggregation promotion of fibrinolysis inhibition of neutrophil response to various stimuli involved in the inflammatory process stabilization lysosomal membranes Cardiovascular effects include the lowering of cholesterol levels, and the inhibition of platelet aggregation. This is of great significance in preventing atherosclerosis and its complication. Curcumin’s cholesterol-lowering actions include interfering with intestinal cholesterol uptake, increasing the conversion ofcholesterol in to bile acids by increasing the activity of hepatic cholesterol-7-alpha-hydroxylase, the rate-limiting enzyme of bile acid synthesis; and increasing the excretion of bile acids via its choleretic effects. Hepatic effects are similar to that of glycyrrhizin and silymarin against carbon tetrachloride and galactosamine-induced liver injury. The antioxidant and hepatoprotective effects alone would support turmeric’s historical use in liver disorders; however, turmeric and curcumin also exert anti-inflammatory and choleretic effects. The increases of SGOT and SGPT commonly seen in experimental models of inflammation have been prevented by curcumin. Curcumin is an active choleretic, increasing bile acid output by over 100%. In addition to increasing biliary excretion ofbile salts, cholesterol, and bilirubin, curcumin also increases the solubility of the bile. This suggests a benefit in the prevention and treatment of cholelithiasis. Gastrointestinal effects: Turmeric’s long use as a carminative has significant research support. Specifically, curcumin has been shown to inhibit gas formation by clostridium perfringens. Turmeric and curcumin have been shown to increase the mucin content of the stomach and exert gastroprotective effects against ulcer formation induced by stress, alcohol, indomethacin, pyloric ligation, and reserpine. Turmeric and curcumin have several clinical applications. Most notable are: · Cancer prevention and treatment adjunct · Inflammation · Atherosclerosis · Liver disorders · Cholelithiasis · Irritable bowel syndrome Curcumin 95% - Clinical Trials, Curcumin, derived from tumeric. (See below for information about HIV) 1. Christopher Ireson et.al. 2001 Characterization of metabolites of the chemopreventive agent Curcumin in human and rat hepatocytes and in the rat in Vivo, and evaluation of their ability to inhibit phorbol ester-induced prostaglandin E2 production Cancer Research 61-1058-1064, February 2001. 2. Kawamori et.al. 1999 Chemopreventive effect of curcumin, a naturally occurring anti- inflammatory agent, during the promotion/progression stages of colon cancer. Cancer Res.59: 597-60 3. Ciolino H P et.al. 1998 Effect of curcumin on the aryl hydrocarbon receptor and cytochrome p450 IAI in MCF 7 human breast carcinoma cells. Biochem pharmacol. 56: 197-206. 4. Cheng A L et.al. 1998 Phase I chemoprevention clinical trial of curcumin. Proc. Am. Soc.Clin. Oncol. 17: 558 a. 5. John M Mariadason et.al. 2000 Genetic re-programming in pathways of colonic cell maturation induced by short chain fatty acids: comparison with trichostatin A, Sulindac and Curcumin and implications for chemoprevention of colon cancer. Cancer Research 60, 4561-4572, August 15, 2000. 6. Huang M.-T. et al. 1992 Effect of dietary curcumin and ascorbyl palmitate on azoxymethane- induced colonic epithelial cell proliferation and focal areas of dysplasia. Cancer Lett. 64:117-121, 1992 7. Rao C.V., Rivenson A. et.al. 1995 Chemoprevention of colon carcinogenesis by dietary curcumin,a naturally occurring plant phenolic compound. Cancer Res.55:259-266. 8. Hanif R. et al. 1997 Curcumin, a natural plant phenolic food additive, inhibits cell proliferation and induces cell cycle changes in colon adenocarcinoma cell lines by a prostaglandin-independent pathway. J.Lab.Clin.Med. 130: 576-584, 1997. 9. Chang F. et.al. 1999 Curcumin inhibits cyclooxygenase-2 transcription in bile-acid and phorbol ester treated human gastrointestinal epithelial cells. Carcinogenesis (Lond) 20: 445-451. 10.Khafif A. et al. Quantitation of chemoprevention synergism between epigallocatechin 3 gallate and curcumin in normal, premalignant and malignant human oral epithelial cells. Carcinogenesis (Lond) 19: 419-424,1998. 11.Ewa Sikora et.al.(Poland) 1997 Inhibition of proliferation and adoptosis of human and rat T.Lmphocytes by curucmin, a curry pigment. Biochem.Pharmacol.54:899-907, 1997. 12.Mazumdar A, Raghavan K, Weinstein J. et.al. 1995 Inhibition of human immunodeficiency virus type-1 integrase by curcumin. Biochem.Pharmacol. 49:1165-1170, 1995 Alzheimer's? By E. J. Mundell NEW YORK (Reuters Health) - Diets rich in curcumin--a compound found in the curry spice turmeric--may help explain why rates of Alzheimer's disease are much lower among the elderly in India compared with their Western peers. Alzheimer's disease is characterized by the buildup of amyloid protein ``plaques'' within the brain. In studies in rats, curcumin ``not only reduces the amyloid, but also reduces the (brain's) response to the amyloid,'' according to researcher Dr. Sally Frautschy of the University of California, Los Angeles. She presented her findings Thursday at the annual meeting of the Society for Neuroscience in San Diego, California. Previous studies have noted that elderly individuals living in Indian villages appear to have the lowest incidence of Alzheimer's disease in the world, with just 1% of those aged 65 and older contracting the degenerative brain condition. The reasons for this low incidence remain unclear, however. Frautschy speculated that curcumin found in curry could provide a clue to this puzzle since the compound has ``a long history of dietary and herbal medicinal use'' and is also a powerful antioxidant and anti-inflammatory agent. In her study, Frautschy fed middle-aged (9 months old) and aged (22 months old) rats diets rich in curcumin. All of the rats had received brain injections of amyloid to mimic progressive Alzheimer's disease. ``Curcumin reduced the accumulation of beta-amyloid and the associated loss of proteins'' in the synapses, or gaps, between individual brain cells, Frautschy reported. ``Synapses connect nerve cells and are crucial for memory,'' the California researcher explained. Keeping synapses free of plaque is important because ``their loss correlates well with memory decline in Alzheimer's.'' This type of memory preservation may have been reflected in the fact that rats fed curcumin also performed much better in memory-dependent maze tests compared with rats on normal diets, according to Frautschy. Curcumin also appeared to reduce Alzheimer's-related inflammation in neurologic tissue. Because ``a combined anti-inflammatory and antioxidant approach will be useful for Alzheimer's prevention or treatment,'' Frautschy speculates that curcumin could be especially valuable in the fight against the disease, especially in combination with anti-inflammatory drugs like ibuprofen. Her team is hopeful they will soon receive funding for clinical trials to investigate curcumin-ibuprofen combination therapy. Curcumin may not be the only compound in the kitchen spice rack able to ward off Alzheimer's. In an interview with Reuters Health, Frautschy said that ``chemicals from rosemary (rosmarinic acid) and ginger (vanillin and zingerone, also high in Indian diets) have similar structure and should be tested.'' Summary of Study: Curcumin Reduces Oxidative Damage and Amyloid Pathology in an Alzheimer Transgenic Mouse. Lim GP, Chu T, Yang F, Beech W, Frautschy SA, Cole GM. Curcumin also known as Turmeric induces cancer cell programmed death better than selenium, vitamin A, vitamin D3, or green tea. In a study of 18 HIV patient receiving 2000 mg of curcumin for 20 weeks the patients had a significant increase in the CD-4 and CD-8 as compared to the patients receiving a placebo. Caution curcumin also lowers cholesterol levels by increasing the flow of bile out of the liver so those with a biliary tract obstruction should not use curcumin. [Life Extension Dec. 1997 pages 16,29,33] [Life Extension June 1997 page 16]. In an animal and in vitro study curcumins were shown to inhibit cancer at initiation, promotion and progressive stages of development. [Nagabhushan m, Bhide SV. Curcumin as an inhibitor of cancer.J Am Cell Nutr 11(2): 192-8, 1992][Botanical Influences on Illness. In animal and in vitro studies curcumins were shown to inhibit cancer cells at initiation, promotion and progression stages of cancer development. [Nagabhushan M, Bhide SV. Curcumin as an inhibitor of cancer. Journal Am Coll Nutr. 11(2):192-8, 1992]. Therapeutic potential of curcumin in human prostate cancer. II. Curcumin inhibits tyrosine kinase activity of epidermal growth factor receptor and depletes the protein Purpose: In a search for alternative and preventive therapies for prostate cancer, attention was focused on the ways in which curcumin (Turmeric), used in food and medicine in India for centuries, could interfere with the growth factor signaling pathways in both androgen-dependent and androgen-independent prostate cancer cells, as exemplified by the epidermal growth factor receptor (EGF-R) signaling. Materials and Methods: The androgen-sensitive LNCaP and androgen-insensitive PC-3 cell lines were grown in 5 to 50 &mgr;M curcumin and analyzed for EGF-R protein by Western blotting and for EGF-R tyrosine kinase activity. Results: Curcumin was a potent inhibitor of EGF-R signaling, and it accomplished this effect by three different means (1) down regulating the EGF-R protein; (2) inhibiting the intrinsic EGF-R tyrosine kinase activity; and (3) inhibiting the ligand-induced activation of the EGF-R. Conclusions: These results, taken together with our previous results that curcumin can induce apoptosis in both androgen-dependent and androgen-independent prostate cancer cells, support our view that curcumin may be a novel modality by which one can interfere with the signal transduction pathways of the prostate cancer cell and prevent it from progressing to its hormone-refractory state. Mol Urol 2000 Spring;4(1):1-6 Curcumin is a major component of the Curcuma species, which is commonly used as a yellow coloring and flavoring agent in foods. Curcumin has shown anti-carcinogenic activity in animals as indicated by its ability to block colon tumor initiation by azoxymethane and skin tumor promotion induced by phorbol ester TPA. Recently, curcumin has been considered by oncologists as a potential third generation cancer chemopreventive agent, and clinical trials using it have been carried out in several laboratories. Curcumin possesses anti-inflammatory activity and is a potent inhibitor of reactive oxygen-generating enzymes, such as lipoxygenase/cyclooxygenase, xanthine dehydrogenase/oxidase and induc-ible nitric oxide synthase. Curcumin is also a potent inhibitor of protein kinase C, EGF-receptor tyrosine kinase and I B kinase. In addition, curcumin inhibits the activation of NF B and the expression of c-jun, c-fos, c-myc and iNOS. It is proposed that curcumin may suppress tumor promotion by blocking signal transduction pathways in the target cells. Curcumin was first biotransformed to dihydrocurcumin and tetrahydrocurcumin, and these compounds were subsequently converted into monoglucuronide conjugates. The experimental results suggest that curcumin-glucuronide, dihydrocurcumin-glucuronide, tetrahydrocurcumin-glucuronide and tetrahydrocurcumin are major metabolites of curcumin in mice.
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