• New research showed that curcumin, the active ingredient in the curry spice turmeric, possesses potent anti-inflammatory and anti-arthritic properties.
• A highly bioavailable form of curcumin was more effective in alleviating rheumatoid arthritis (RA) symptoms than the NSAID drug Voltaren
• While no one in the curcumin group withdrew from the study due to side effects, 14 percent of those in the NSAID group did so, as NSAIDs often cause serious adverse effects, including ulcers and heart problems

About Curcumin

There are several data in the literature indicating a great variety of pharmacological activities of Curcuma longa L. (Zingiberaceae), which exhibit anti-inflammatory, anti-human immunodeficiency virus, anti-bacteria, antioxidant effects and nematocidal activities. Curcumin is a major component in Curcuma longa L., being responsible for its biological actions. Other extracts of this plant has been showing potency too.
In vitro, curcumin exhibits anti-parasitic, antispasmodic, anti-inflammatory and gastrointestinal effects; and also inhibits carcinogenesis and cancer growth. In vivo, there are experiments showing the anti-parasitic, anti-inflammatory potency of curcumin and extracts of C. longa L. by parenteral and oral application in animal models [1].

Dr. Marion Chan’s laboratory[2]

Dr. Marion Chan’s laboratory is interested in understanding mechanisms that resolve inflammation. She and her team have developed two model systems in mice which, in combination, allows study of these mechanism at the cellular and the whole organism levels. This work has implications for a wide spectrum of disease states, which is now thought to involve a chronic neuroinflammatory response.

Chan’s laboratory was the first to show that there is an active mechanism of resolution underlying remission and relapse in murine collagen-induced arthritis (CIA), a well-accepted model of rheumatoid arthritis in humans. Her findings indicated that COX inhibitors will interfere with the resolution process, resulting in chronic inflammation. (This is a critical issue because COX-2 inhibitors are widely used for treating many inflammatory diseases.) Her current work centers on elucidating the details of this mechanism. The immediate focus is on the eicosanoids synthesized from arachidonic acid through the COX and lipoxygenase (LOX) pathways. Many of these bioactive lipids are ligands for peroxisome proliferator-activated receptor (PPAR), a group of nuclear factors that serve as targets for diabetes, obesity, vascular disease, and other inflammatory diseases.

One of the characteristics of PPARγ is that it primes monocytes to differentiate into alternatively activated M2 phenotype. This subclass of macrophages expresses scavenger receptors for apoptotic cells, produces transforming growth factor β and IL-10, and has been ascribed vital roles in the clearance of apoptotic neutrophils and wound repair. They are likely the initiators of resolution, in contrast to the classically activated macrophages (M1) that induce inflammation.

The second murine model of inflammation looks at leishmaniasis, a parasitic infection that produces inflammation and affects 12 million people worldwide. The etiological agent is a parasitic protozoan that infects the bone marrow, liver, skin, and spleen of susceptible individuals chronically. The parasite lives and replicates within macrophages. The Chan group is investigating whether the parasite harnesses resolution mechanisms to maintain the life-long infection. The hypothesis is that, upon infection, Leishmania polarizes macrophages towards the alternatively activated M2 phenotype that produce arginase, instead of the classically activated M1 macrophages that express inducible nitric oxide synthase. Consequently, arginine, the common substrate of the two enzymes, diverge from producing the parasiticidal nitric oxide. Among the dietary compounds studied in the laboratory, curcumin is a PPARγ activator and agonist. This anti-inflammatory molecule increases parasite burden in Leishmania donovani-infected mice.

Tips for Increasing Your Absorption of Curcumin [3]

• If you want to give curcumin a try for RA, it is widely available in supplement form, but relatively high doses are required to achieve its therapeutic effects, and curcumin is generally not absorbed that well. Typical therapeutic doses are up to three grams of bioavailable curcumin extract, three to four times daily, and this is difficult to achieve using standard curcumin powders.
• One alternative is to make a microemulsion by combining a tablespoon of curcumin powder with 1-2 egg yolks and a teaspoon or two of melted coconut oil. Then use a hand blender on high speed to emulsify the powder.
• Another strategy you can use to increase absorption is to put one tablespoon of the curcumin powder into a quart of boiling water. It must be boiling when you add the powder, as it will not work as well if you put it in room temperature water and heat the water and curcumin together.
• After boiling it for 10 minutes you will have created a 12% solution and you can drink this once it has cooled down. The curcumin will gradually fall out of the solution over time and in about six hours it will be a 6% solution, so it is best to drink the water within four hours. It does have a woody taste, but this is done more for therapeutic benefits than flavor.

About Cyclooxygenases (COXs)

Cyclooxygenases (COXs), also known as prostaglandin H synthases, are fatty acid oxygenases that contain about 600 amino acid residues and act on arachidonic acid to generate prostaglandins (PG). All vertebrates contain two COX genes: one encoding the constitutive COX-1 and another inducible COX-2. COX-1 and COX-2 share approximately 60-65% amino acid identity. These COX isoforms are bifunctional hemoproteins that catalyze both the bioxygenation of arachidonic acid to form PGG2 and the peroxidative reduction of PGG2 to form PGH2. Hence, the catalytic domain of COX is considered to contain both cyclooxygenase and peroxidase active sites. The peroxidase site is required for the activation of heme groups that participate in the cyclooxygenase reaction.

About growth factor-beta and interleukin-10

Contextual regulation of inflammation: a duet by transforming growth factor-beta and interleukin-10
Transforming growth factor-beta (TGF-beta) and interleukin-10 (IL-10) are regulatory cytokines with pleiotropic roles in the immune system. The prominent function of TGF-beta is to maintain T cell tolerance to self or innocuous environmental antigens via its direct effects on the differentiation and homeostasis of effector and regulatory T cells. A critical route for the regulation of T cells by TGF-beta is via activation of a T cell-produced latent form of TGF-beta1 by dendritic cell-expressed avbeta8 integrin. IL-10 operates primarily as a feedback inhibitor of exuberant T cell responses to microbial antigens. T cells are also the principal producers of IL-10, the expression of which is regulated by IL-27, IL-6, and TGF-beta. The collective activity of TGF-beta and IL-10 ensures a controlled inflammatory response specifically targeting pathogens without evoking excessive immunopathology to self-tissues [4].

1. Biological activities of Curcuma longa L. Araújo CC, Leon LL. Laboratório de Biologia de Tripanosomatídeos, Instituto Oswaldo Cruz-Fiocruz, 21045-900 Rio de Janeiro, RJ, Brasil. cacaraujo@hotmail.com
2. Chan
Chan MM, Huang HI, Mattiacci JA, Fong D. Modulation of cytokine gene expression by curcumin. In “Food Factors in Health Promotion and Disease Prevention”, ed. Shahidi F, Ho C-T, Watanabe S, Osawa T. American Chemical Society Press, Washington D.C., pp. 86-99, 2003.
Chan MM, Fong D. Modulation of the nitric oxide pathway by natural products. In Nitric Oxide in Inflammation and Tissue Injury (Laskin J, Laskin D, eds.). Marcel Dekker, Inc., New York, NY, 1999.
Chan MM. Inhibition of tumor necrosis factor by curcumin, a phytochemical. Biochem Pharmacol. 1995 May 26;49(11):1551-6.
Chan MM, Fong D. 1994. Anti-inflammatory and cancer preventive immuno-modulation through the diet: The effects of curcumin on T lymphocytes. In “Food Phytochemicals for Cancer Prevention”, ed. Huang M-T, Ho C-T, American Chemical Society Press, Washington D.C., pp. 222-230.
Chan MM, Fong D. Plant microtubule inhibitors against trypanosomatids. Parasitol Today. 1994 Nov;10(11):448-51.
Chan MM, Grogl M, Chen CC, Bienen EJ, Fong D. Herbicides to curb human parasitic infections: in vitro and in vivo effects of trifluralin on the trypanosomatid protozoans. Proc Natl Acad Sci U S A. 1993 Jun 15;90(12):5657-61.
Chan MM. T cell response in murine Leishmania mexicana amazonensis infection: production of interferon-gamma by CD8+ cells. Eur J Immunol. 1993 May;23(5):1181-4.
Chan MM, Fong D. Inhibition of leishmanias but not host macrophages by the antitubulin herbicide trifluralin. Science. 1990 Aug 24;249(4971):924-6.
Recent Medically Related Publications, Obtained from PubMed (Click on PubMed ID to view abstract)

22536211. Chan MM, Fong D, The Interplay of PPARs with Parasites and Related Intracellular Pathogens. PPAR Res 2012:(624845)2012

22448168. Chan MM, Adapala N, Chen C, Peroxisome Proliferator-Activated Receptor-?-Mediated Polarization of Macrophages in Leishmania Infection. PPAR Res 2012:(796235)2012

20435922. Chan MM, Moore AR, Resolution of inflammation in murine autoimmune arthritis is disrupted by cyclooxygenase-2 inhibition and restored by prostaglandin E2-mediated lipoxin A4 production. J Immunol 184:11(6418-26)2010 Jun 1

20169106. Chan MM, Evans KW, Moore AR, Fong D, Peroxisome proliferator-activated receptor (PPAR): balance for survival in parasitic infections. J Biomed Biotechnol 2010:(828951)2010

18794851. Adapala N, Chan MM, Long-term use of an antiinflammatory, curcumin, suppressed type 1 immunity and exacerbated visceral leishmaniasis in a chronic experimental model. Lab Invest 88:12(1329-39)2008 Dec

16402374. Chan MM, Soprano KJ, Weinstein K, Fong D, Epigallocatechin-3-gallate delivers hydrogen peroxide to induce death of ovarian cancer cells and enhances their cisplatin susceptibility. J Cell Physiol 207:2(389-96)2006 May

15772867. Chan MM, Adapala NS, Fong D, Curcumin overcomes the inhibitory effect of nitric oxide on Leishmania. Parasitol Res 96:1(49-56)2005 Apr

12632163. Chan MM, Bulinski JC, Chang KP, Fong D, A microplate assay for Leishmania amazonensis promastigotes expressing multimeric green fluorescent protein. Parasitol Res 89:4(266-71)2003 Mar

12447990. Chan MM, Fong D, Soprano KJ, Holmes WF, Heverling H, Inhibition of growth and sensitization to cisplatin-mediated killing of ovarian cancer cells by polyphenolic chemopreventive agents. J Cell Physiol 194:1(63-70)2003 Jan

11841782. Chan MM, Antimicrobial effect of resveratrol on dermatophytes and bacterial pathogens of the skin. Biochem Pharmacol 63:2(99-104)2002 Jan 15

11020457. Chan MM, Mattiacci JA, Hwang HS, Shah A, Fong D, Synergy between ethanol and grape polyphenols, quercetin, and resveratrol, in the inhibition of the inducible nitric oxide synthase pathway. Biochem Pharmacol 60:10(1539-48)2000 Nov 15

9714315. Chan MM, Huang HI, Fenton MR, Fong D, In vivo inhibition of nitric oxide synthase gene expression by curcumin, a cancer preventive natural product with anti-inflammatory properties. Biochem Pharmacol 55:12(1955-62)1998 Jun 15

9393670. Chan MM, Fong D, Ho CT, Huang HI, Inhibition of inducible nitric oxide synthase gene expression and enzyme activity by epigallocatechin gallate, a natural product from green tea. Biochem Pharmacol 54:12(1281-6)1997 Dec 15
3. http://articles.mercola.com/sites/articles/archive/2012/06/13/the-spice-that-is-better-than-drugs-for-ra.aspx
4. Li MO, Flavell RA. Immunology Program, Memorial Sloan-Kettering Cancer Center, New York, NY 10065, USA. lim@mskcc.org

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