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Curcumin / Turmeric
Biological activities of curcumin and its analogues (Congeners) made by man and Mother Nature.
Anand Biochem Pharmacol. 2008 Aug 19. [Epub ahead of print]
P, Thomas SG, Kunnumakkara AB, Sundaram C, Harikumar KB, Sung B, Tharakan ST, Misra KP, Priyadarsini IK, Rajasekharan KN, Aggarwal BB.
Cytokine Research Laboratory, Department of Experimental Therapeutics, Unit 143, The University of Texas M.D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX 77030, USA.
Curcumin, a yellow pigment present in the Indian spice turmeric (associated with curry powder), has been linked with suppression of inflammation; angiogenesis; tumorigenesis; diabetes; diseases of the cardiovascular, pulmonary, and neurological systems, of skin, and of liver; loss of bone and muscle; depression; chronic fatigue; and neuropathic pain.
The utility of curcumin is limited by its color, lack of water solubility, and relatively low in vivo bioavailability. Because of the multiple therapeutic activities attributed to curcumin, however, there is an intense search for a "super curcumin" without these problems. Multiple approaches are being sought to overcome these limitations. These include discovery of natural curcumin analogues from turmeric; discovery of natural curcumin analogues made by Mother Nature; synthesis of "man-made" curcumin analogues; reformulation of curcumin with various oils and with inhibitors of metabolism (e.g., piperine); development of liposomal and nanoparticle formulations of curcumin; conjugation of curcumin prodrugs; and linking curcumin with polyethylene glycol. Curcumin is a homodimer of feruloylmethane containing a methoxy group and a hydroxyl group, a heptadiene with two Michael acceptors, and an alpha,beta-diketone. Structural homologues involving modification of all these groups are being considered. This review focuses on the status of all these approaches in generating a "super curcumin.".
Curcumin as Alzheimer and Cancer preventive
Curcumin has been used for thousands of years as a medicinal preparation made from turmeric or as turmeric powder used as a preservative and coloring agent in foods (yellow curry powder). Curcumin was isolated as the major yellow pigment in turmeric, a pure chemical (diferulomethane). Curcumin’s structure is similar to other plant pigments called polyphenolics (chemicals containing muliple “phenol” groups) which often have potent anti-oxidant and anti-inflammatory properties and associated health benefits. Many similar plant pigments are known as potent antioxidants, for example, the pigments extracted from grapes in red wine (resveratrol), or in green tea (catechins) or in fruit juices (blueberries, strawberries, pomegranates etc) typically contain polyphenolic antioxidants and have been studied for their possible medicinal or preventive value.
Curcumin, a polyphenol, is unique for the many reasons
Curcumin is the Asian version of aspirin. Our wonder drug aspirin was originally purifed from willow bark extracts that were used in European and American Indian traditional medicines to control inflammation. Eventually aspirin was synthesized by German chemists and developed by Bayer as one of the most successful drugs in the Western medicine cabinet. Today aspirin is used not only in pain remedies and other analgesic applications, but to control minor fever and inflammation and, at low doses, to prevent heart attack and stroke. Curcumin has been used in traditional Indian (Ayruvedic) and Chinese medicine for thousands of years largely because of its proven efficacy in treating conditions with inflammation. They also used it in foods as an effective food preservative, just as we use synthetic additives like BHA. These ancient civilizations have vast trial and error experience with many different herbal remedies and food preparations and they selected curcumin as a food additive and major tool for medicinal use based on efficacy- not superstition.
Curcumin as a possible cure for Alzheimer
Curcumin and Alzheimer’s Disease. Scientists has tested curcumin in several models for Alzheimer’s and found that it not only reduces oxidative damage and inflammation (as expected), but also reduces amyloid accumulation and synaptic marker loss and promotes amyloid phagocytosis and clearance. Curcumin worked to prevent synaptic marker and cognitive deficits caused by amyloid peptide infusion and abeta oligomer toxicity in vitro. The work on curcumin and AD is discussed in detail in PubMed publications.
Curcumin structure-function, bioavailability, and efficacy in models of neuroinflammation and Alzheimer
Begum AN, Jones MR, Lim GP, Morihara T, Kim P, Heath DD, Rock CL, Pruitt MA, Yang F, Hudspeth B, Hu S, Faull KF, Teter B, Cole GM, Frautschy SA.
Department of Medicine, University of California, Los Angeles, California, USA.
Curcumin can reduce inflammation and neurodegeneration, but its chemical instability and metabolism raise concerns, including whether the more stable metabolite tetrahydrocurcumin (TC) may mediate efficacy. We examined the antioxidant, anti-inflammatory, or anti-amyloidogenic effects of dietary curcumin and TC, either administered chronically to aged Tg2576 APPsw mice or acutely to lipopolysaccharide (LPS)-injected wild-type mice. Despite dramatically higher drug plasma levels after TC compared with curcumin gavage, resulting brain levels of parent compounds were similar, correlating with reduction in LPS-stimulated inducible nitric-oxide synthase, nitrotyrosine, F2 isoprostanes, and carbonyls. In both the acute (LPS) and chronic inflammation (Tg2576), TC and curcumin similarly reduced interleukin-1beta. Despite these similarities, only curcumin was effective in reducing amyloid plaque burden, insoluble beta-amyloid peptide (Abeta), and carbonyls. TC had no impact on plaques or insoluble Abeta, but both reduced Tris-buffered saline-soluble Abeta and phospho-c-Jun NH(2)-terminal kinase (JNK). Curcumin but not TC prevented Abeta aggregation. The TC metabolite was detected in brain and plasma from mice chronically fed the parent compound. These data indicate that the dienone bridge present in curcumin, but not in TC, is necessary to reduce plaque deposition and protein oxidation in an Alzheimer's model. Nevertheless, TC did reduce neuroinflammation and soluble Abeta, effects that may be attributable to limiting JNK-mediated transcription. Because of its favorable safety profile and the involvement of misfolded proteins, oxidative damage, and inflammation in multiple chronic degenerative diseases, these data relating curcumin dosing to the blood and tissue levels required for efficacy should help translation efforts from multiple successful preclinical models.
The curry spice curcumin reduces oxidative damage and amyloid pathology in an Alzheimer transgenic mouse.
Lim GP, Chu T, Yang F, Beech W, Frautschy SA, Cole GM. J Neurosci. 2001 Nov 1;21(21):8370-7. Links
Departments of Medicine and Neurology, University of California, Los Angeles, Los Angeles, California 90095, USA.
Inflammation in Alzheimer's disease (AD) patients is characterized by increased cytokines and activated microglia. Epidemiological studies suggest reduced AD risk associates with long-term use of nonsteroidal anti-inflammatory drugs (NSAIDs). Whereas chronic ibuprofen suppressed inflammation and plaque-related pathology in an Alzheimer transgenic APPSw mouse model (Tg2576), excessive use of NSAIDs targeting cyclooxygenase I can cause gastrointestinal, liver, and renal toxicity. One alternative NSAID is curcumin, derived from the curry spice turmeric. 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 of dietary curcumin (5000 ppm) on inflammation, oxidative damage, and plaque pathology. Low and high doses of curcumin 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.
Alzheimer study