Natural Yellow 3
Curcumin is the active ingredient of the Indian curry spice turmeric.
It is a polyphenol
with a molecular formula C21H20O6. Curcumin can
exist in at least two tautomeric
forms, keto and
enol. The keto form
is preferred in solid phase and the enol form in solution.
Curcumin can be used for boron quantification in the so-called curcumin
method. It reacts with boric
acid forming a red colored compound, known as rosocyanine.
Curcumin is known for its antitumor, antioxidant,
properties. Anti-inflammatory action may be due to leukotriene inhibition.
Curcumin acts as a free radical scavenger and antioxidant, inhibiting lipid
peroxidation and oxidative DNA damage. Curcuminoids induce glutathione
S-transferase and are potent inhibitors of cytochrome
For the last few decades, extensive work has been done to establish the
biological activities and pharmacological actions of curcumin. Its anticancer
effects stem from its ability to induce apoptosis
in cancer cells without cytotoxic effects on healthy cells. Curcumin can
interfere with the activity of the transcription factor NF-κB ( NF-kB
), which is often highly overexpressed in many cancer cells, according to a talk
given by Dr. Dennis
Liotta at Davidson
College in January 2006.
A 2004 UCLA-Veterans Affairs study involving genetically altered mice
suggests that curcumin might inhibit the accumulation of destructive beta-amyloid
in the brains of Alzheimer's
disease patients and also break up existing plaques associated with the
disease. It was published that curcumin inhibits cyclooxygenase-2
(COX-2) as well as lipoxygenase
(LOX), two enzymes involved in inflammation.
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Curcumin is the principal curcuminoid of the popular Indian spice turmeric, which is a member of the ginger family (Zingiberaceae). Turmeric's other two curcuminoids are desmethoxycurcumin and bis-desmethoxycurcumin. The curcuminoids are natural phenols that are responsible for the yellow color of turmeric. Curcumin can exist in several tautomeric forms, including a 1,3-diketo form and two equivalent enol forms. The enol form is more energetically stable in the solid phase and in solution.
Curcumin can be used for boron quantification in the curcumin method. It reacts with boric acid to form a red-colored compound, rosocyanine.
Curcumin is brightly yellow colored and may be used as a food coloring. As a food additive, its E number is E100.
Curcumin incorporates several functional groups. The aromatic ring systems, which are phenols, are connected by two α,β-unsaturated carbonyl groups. The diketones form stable enols and are readily deprotonated to form enolates; the α,β-unsaturated carbonyl group is a good Michael acceptor and undergoes nucleophilic addition. The structure was first identified in 1910 by J. Miłobędzka, Stanisław Kostanecki and Wiktor Lampe.
Curcumin is used as an indicator for boron.
The biosynthetic route of curcumin has proven to be very difficult for researchers to determine. In 1973 Roughly and Whiting proposed two mechanisms for curcumin biosynthesis. The first mechanism involved a chain extension reaction by cinnamic acid and 5 malonyl-CoA molecules that eventually arylized into a curcuminoid. The second mechanism involved two cinnamate units being coupled together by malonyl-CoA. Both mechanisms use cinnamic acid as their starting point, which is derived from the amino acid phenylalanine. This is noteworthy because plant biosyntheses employing cinnamic acid as a starting point are rare compared to the more common use of p-coumaric acid. Only a few identified compounds, such as anigorufone and pinosylvin, use cinnamic acid as their start molecule. An experimentally backed route was not presented until 2008. This proposed biosynthetic route follows both the first and second mechanisms suggested by Roughley and Whiting. However, the labeling data supported the first mechanism model in which 5 malonyl-CoA molecules react with cinnamic acid to form curcumin. However, the sequencing in which the functional groups, the alcohol and the methoxy, introduce themselves onto the curcuminoid seems to support more strongly the second proposed mechanism. Therefore, it was concluded the second pathway proposed by Roughly and Whiting was correct.
Potential medical uses
Although many preclinical studies suggest curcumin may be useful for the prevention and treatment of several diseases, the effectiveness of curcumin has not yet been demonstrated in randomized, placebo-controlled, double-blind clinical trials.
A daily dose of 2 grams of Curcuma domestica extract was found to provide pain relief that was equivalent to ibuprofen for the relief of pain associated with osteoarthritis of the knee. An extensive survey of the literature shows a number of other potential uses and that daily doses over a 3 month period of up to 12 grams proved safe. Some commercial capsules of curcumin contain piperine, a compound found in pepper which aids absorption of curcumin into the blood stream. However, as curcuma is known to inhibit blood clotting, it should be avoided for a two week period prior to major surgery and not used in conjunction with blood thinners such as warfarin and Plavix. It is also known to aggravate gallstone problems.
Turmeric has been used historically as a component of Indian Ayurvedic medicine. Research in the latter half of the 20th century identified curcumin as the agent responsible for most of the biological activity of turmeric. In vitro and animal studies have suggested a wide range of potential therapeutic or preventive effects associated with curcumin. At present, these effects have not been confirmed in humans. As of 2008, numerous clinical trials in humans were underway, studying the effect of curcumin on various diseases, including multiple myeloma, pancreatic cancer, myelodysplastic syndromes, colon cancer, psoriasis, and Alzheimer's disease.
In both in vitro and animal studies, curcumin has shown antitumor, antioxidant, antiarthritic, antiamyloid, anti-ischemic, and anti-inflammatory properties.
Anti-inflammatory properties may be due to inhibition of eicosanoid biosynthesis.
There is a study that demonstrated that curcumin may be an alternative antimicrobial agent against fatal bacterial infections including Vibrio vulnificus infection. In the study, curcumin protected mice from V. vulnificus-induced septicemia.
In HIV, it appears to act by interfering Curcumin P300/CREB-binding protein (CBP).
A study found it hepatoprotective in combination with Absinthium in rats.
A study found that low concentrations of Curcumin interfere with Herpes simplex virus-1 (HSV-1) replication. It inhibited the recruitment of RNA polymerase II to viral DNA, thus inhibiting its transcription. This effect was independent of the effect on histone acetyltransferase activities of p300/CBP.
A study found that curcumin is significantly associated with protection from infection by HSV-2 in animal models of intravaginal infections.
A study found that curcumin acts as a free radical scavenger and antioxidant, inhibiting lipid peroxidation and oxidative DNA damage, protecting against lead neurotoxicity, in rats.
Curcuminoids induce glutathione S-transferase and are potent inhibitors of cytochrome P450
Curcumin was shown to be effective in protecting against toxicity and spatial memory impairment induced by amyloid β-protein infusion in a rat model.
A study using a transgenic animal model indicated that curcumin diminished plaque burden and overall inflammation, but it also increased plaque-associated inflammatory cells suggesting enhanced clearance.
A study found that Curcumin shrank the size of plaques and reduced neurite dystrophy in an Alzheimer mouse model.
A study found Curcumin to have a synergistic effect with fish oil to protect against cognitive deficits in a transgenic rodent model.
However, the results of studies in rodents may not translate to humans. In humans, unlike rats, curcumin is extensively metabolized to the glucuronidated form, which does not penetrate the blood–brain barrier and is therefore unable to reach brain tissues.
Numerous studies have demonstrated that curcumin has a positive effect on neurogenesis in the hippocampus and increases the levels of brain-derived neurotrophic factor (BDNF) in rats.
A curcumin pyrazole derivative identified by high throughput screening was found to improve memory and was broadly neuroprotective, stimulating BDNF in vitro and in vivo. The compound was found to be protective in animal models of brain trauma and stroke.
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Its potential anticancer effects stem from its ability to induce apoptosis in cancer cells without cytotoxic effects on healthy cells. Curcumin can interfere with the activity of the transcription factor NF-κB, which has been linked to a number of inflammatory diseases such as cancer.
A 2009 study suggested curcumin may inhibit mTOR complex I via a novel mechanism.
Another 2009 study on curcumin effects on cancer states it "modulates growth of tumor cells through regulation of multiple cell signaling pathways including cell proliferation pathway (cyclin D1, c-myc), cell survival pathway (Bcl-2, Bcl-xL, cFLIP, XIAP, c-IAP1), caspase activation pathway (caspase-8, 3, 9), tumor suppressor pathway (p53, p21) death receptor pathway (DR4, DR5), mitochondrial pathways, and protein kinase pathway (JNK, Akt, and AMPK)".
An in vitro study in a human glioblastoma cell line reported that curcumin effectively inhibits tumor cell proliferation, as well as migration and invasion, and that these effects may be mediated through interference with the STAT3 signaling pathway.
When 0.2% curcumin is added to diet given to rats or mice previously given a carcinogen, it significantly reduces colon carcinogenesis.
In a study curcumin has been shown in vitro to have phyto-estrogenic activity that might contribute to activity against breast cancer.
In immunodeficient mice with breast cancer, curcumin inhibited the formation of lung metastases  probably through the NF-κB dependent regulation of protumorigenic inflammatory cytokines.
A study found that curcumin might be potentially useful in some kidney diseases by reducing lipopolysaccharide-induced renal inflammation.
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