turmeric extract research
Turmeric Extract: its medicinal properties are attributed partly to its anti-oxidant and anti-inflammatory characteristics.
Turmeric extract is a concentrated form of the natural spice which is simply a powdered form of the dried root. Turmeric Extract contains three molecular forms: the methoxy form, the demethoxy form and the bisdemethoxy form. The forms tested in the research articles mentioned below are usually a natural mixture of all three unless otherwise stated.
Turmeric Extract is not toxic even at high doses, in laboratory animals, and has been in customary use by the people of India for centuries. As a food coloring ("Food Color E100") turmeric extract is generally recognised as safe (US FDA). Customary dosages for Turmeric Extract are in the range of 1-2.5 gms per day. Turmeric Extract can be obtained in the market place at purities above 95% which is now the standard.
Turmeric extract has attracted the attention of researchers in the fields of Alzheimer's Disease, Arthritis, Cancer and Diabetes. Selections from recent research articles on the effects of turmeric extract are included below.
|Alzheimer's Disease and Turmeric Extract|
Article 1: "Alzheimer's disease (AD) involves amyloid (Abeta) accumulation, oxidative damage and inflammation, and risk is reduced with increased antioxidant and anti-inflammatory consumption. The phenolic yellow curry pigment curcumin has potent anti-inflammatory and antioxidant activities and can suppress oxidative damage, inflammation, cognitive deficits, and amyloid accumulation. ... When fed to aged Tg2576 mice with advanced amyloid accumulation, (it) labeled plaques and reduced amyloid levels and plaque burden. Hence, (it) directly binds small ss-amyloid species to block aggregation and fibril formation in vitro and in vivo. These data suggest that low dose curcumin effectively disaggregates Ass as well as prevents fibril and oligomer formation, supporting the rationale for (its) use in clinical trials preventing or treating AD."|
J Biol Chem. 2004 Dec 7; Curcumin inhibits formation of Abeta oligomers and fibrils and binds plaques and reduces amyloid in vivo. Yang F, Lim GP, Begum AN, Ubeda OJ, Simmons MR, Ambegaokar SS, Chen PP, Kayed R, Glabe CG, Frautschy SA, Cole GM. GRECC (VA Medical) and Medicine, University of California Los Angeles, North Hills, CA 91343.
Article 2: "... we examined the effects of curcumin (Cur) and rosmarinic acid (RA) on the formation, extension, and destabilization of fAbeta(1-40) and fAbeta(1-42) at pH 7.5 at 37 degrees C in vitro. ... Cur and RA dose-dependently inhibited fAbeta formation from Abeta(1-40) and Abeta(1-42), as well as their extension. In addition, they dose-dependently destabilized preformed fAbetas. ... Although the mechanism by which Cur and RA inhibit fAbeta formation from Abeta and destabilize preformed fAbeta in vitro remains unclear, they could be a key molecule for the development of therapeutics for AD."
Article 3: " ... Curcumin has an extensive history as a food additive and herbal medicine in India and is also a potent polyphenolic antioxidant. To evaluate whether it could affect Alzheimer-like pathology in the APPSw mice, we tested a low (160 ppm) and a high dose ... on inflammation, oxidative damage, and plaque pathology. Low and high doses of (it) significantly lowered oxidized proteins and interleukin-1beta, a proinflammatory cytokine elevated in the brains of these mice. With low-dose but not high-dose curcumin treatment, the astrocytic marker GFAP was reduced, and insoluble beta-amyloid (Abeta), soluble Abeta, and plaque burden were significantly decreased by 43-50%. However, levels of amyloid precursor (APP) in the membrane fraction were not reduced. Microgliosis was also suppressed in neuronal layers but not adjacent to plaques. In view of its efficacy and apparent low toxicity, this Indian spice component shows promise for the prevention of Alzheimer's disease."
|Arthritis and Turmeric Extract|
Article 1: "The cytokine macrophage migration inhibitory factor (MIF) has recently emerged as a crucial factor in the pathogenesis of rheumatoid arthritis (RA). ... Curcumin and caffeic acid were found to be the most potent inhibitors, exhibiting IC(50) values in the submicromolar range in the ketonase assay. ... Our results reveal MIF as a possible target for the herbal anti-rheumatic agents."
OBJECTIVE: "Therefore, we undertook studies to determine the antiarthritic efficacy and mechanism of action of a well-characterized turmeric extract using an animal model of rheumatoid arthritis (RA). RESULTS: A turmeric fraction depleted of essential oils profoundly inhibited joint inflammation and periarticular joint destruction in a dose-dependent manner... Consistent with these findings, inflammatory cell influx, joint levels of prostaglandin E(2), and periarticular osteoclast formation were inhibited by turmeric extract treatment. CONCLUSION: These translational studies demonstrate in vivo efficacy and identify a mechanism of action for a well-characterized turmeric extract that supports further clinical evaluation of turmeric dietary supplements in the treatment of RA.
|Cancer and Turmeric Extract|
Article 1: "Curcumin, a natural product isolated from the spice turmeric, has been shown to exhibit a wide range of pharmacological activities including certain anti-cancer properties. It has been specifically shown to be an effective inhibitor of angiogenesis both in vitro and in vivo."|
Bioorg Med Chem. 2005 Jun 2;13(12):4007-13. Synthesis and biological evaluation of aromatic enones related to curcumin. Robinson TP, Hubbard RB 4th, Ehlers TJ, Arbiser JL, Goldsmith DJ, Bowen JP. Center for Biomolecular Structure and Dynamics, Department of Chemistry, University of Georgia, Athens, GA 30602, USA.
Article 2: " ... Curcumin, one of the most studied chemopreventive agents, is a natural compound extracted from Curcuma longa L. that allows suppression, retardation or inversion of carcinogenesis. (It) is also described as an anti-tumoral, anti-oxidant and anti-inflammatory agent capable of inducing apoptosis in numerous cellular systems. ..."
|Cancer (colon, bladder and lung) and Turmeric Extract|
Article 1: "The effects of curcumin on the growth of human colon cancer cell lines, HT-29 and WiDr cells were examined ... RESULTS: Curcumin inhibited the growth of HT-29 and WiDr cells in a dose-dependent fashion." |
Korean J Gastroenterol. 2005 Apr;45(4):277-84. [The inhibitory effect of curcumin on the growth of human colon cancer cells (HT-29, WiDr) in vitro] Kim KH, Park HY, Nam JH, Park JE, Kim JY, Park MI, Chung KO, Park KY, Koo JY. Department of Internal Medicine, Kosin University College of Medicine, Busan 602-702, Korea.
Article 2: "CONCLUSIONS: Curcumin can suppress the growth, induce apoptosis of bladder cancer EJ cell in vitro. Its mechanism is related with down-regulations of the expressions of NF-kappaB and Cyclin D1. (It) has great potential for the treatment of bladder cancer."
Article 3: "OBJECTIVE: To investigate the mechanism of anti-tumor effects of curcumin on human lung cancer cell (A549). ... CONCLUSION: Curcumin can interfere with ... growth cycle of A549 cell and suppress cell growth. The suppression effect is concentration dependent. ..."
|Cancer (breast and ovary) and Turmeric Extract|
Article 1: "OBJECTIVE: To study the suppressive effects of curcumin on breast carcinoma cells and the mechanism. RESULTS: (It) inhibits the proliferation in both estrogen receptor (ER) positive MCF-7 cells and ER negative MDA-MB-231 cells. ... In addition, (it) exerts strong anti-invasive effects in vitro which was not estrogen dependent in the ER-negative MDA-MB-231 breast cancer cells. ... CONCLUSION: (It) exerts multiple suppressive effects on breast carcinoma cells; it's mechanism of chemoprevention is pleiotropic."|
Zhonghua Yi Xue Za Zhi. 2003 Oct 25;83(20):1764-8. [Analysis of anti-proliferation of curcumin on human breast cancer cells and its mechanism] Di GH, Li HC, Shen ZZ, Shao ZM. Hospital, Fudan University, Shanghai 200032, China.
Article 2: "The inhibitory effect of curcumin, the yellow-colored pigment from turmeric, on telomerase activity was analyzed in human mammary epithelial (MCF-10A) and breast cancer (MCF-7) cells. ... In MCF-7 cells, telomerase activity decreased with increasing concentrations of (it), inhibiting about 93.4% activity at 100 microM concentration..."
Article 3: "It was concluded that curcumin could significantly inhibit the growth of ovary cancer cells. The induction of apoptosis by down-regulating the expression of bcl-2 and p53 was probably one of its molecular mechanisms."
|Diabetes and Turmeric Extract|
Article 1: "... We tested the hypothesis that the plant polyphenolic compound curcumin, which is known to exert potent antiinflammatory and antioxidant effects, would ameliorate diabetes and inflammation in murine models of insulin-resistant obesity. We found that Curcumin admixture ameliorated diabetes in high-fat diet-induced obese and leptin-deficient ob/ob male C57BL/6J mice as determined by glucose and insulin tolerance testing and hemoglobin A1c percentages. We therefore conclude that orally ingested curcumin reverses many of the inflammatory and metabolic derangements associated with obesity and improves glycemic control in mouse models of type 2 diabetes. ..."
|Melanoma and Turmeric Extract|
Article 1: "Curcumin induced melanoma cell apoptosis and cell cycle arrest, ... Our results demonstrate that (it) arrested cell growth at the G(2)/M phase and induced apoptosis in human melanoma cells by inhibiting NFkappaB activation and thus depletion of endogenous nitric oxide. Therefore, (it) should be considered further as a potential therapy for patients with melanoma."|
Melanoma Res. 2004 Jun;14(3):165-71. Inhibition of nuclear factor-kappaB and nitric oxide by curcumin induces G2/M cell cycle arrest and apoptosis in human melanoma cells. Zheng M, Ekmekcioglu S, Walch ET, Tang CH, Grimm EA. Department of Bioimmunotherapy, The University of Texas MD Anderson Center, Houston, TX 77030, USA.
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Withanolide (from Ashwagandha)
Zerumbone (from Ginger)
|This website acknowledges Pubmed (www.ncbi.nlm.nih.gov) as source for medical research abstracts.|
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