Anti-inflammatory herbs: panax notoginseng and others

panax.JPGPnS has an obvious anti-inflammatory effect and its mechanisms are related to the inhibition of the Neu-[Ca2+]i level and PLA2 activity, and reduction of Din content.

Herbal medicines have traditionally played a major role in the management of diabetes in Asian countries for centuries. Panax notoginseng (Burk) F. H. Chen (Araliaceae) known as Tiánqī or san qi is a well-known medicinal herb in Asia for its long history of use in Chinese medicine. Qualified as ‘the miracle root for the preservation of life’, it has been used in China for 600 years, for treatment of various diseases. Panax notoginseng saponins (PNS) are the key active components. PNS have been widely used in China for treatment of cardiovascular diseases. However, scientific studies have shown a wide range of other pharmacological applications including anti-cancer, neuroprotective and anti-inflammatory agents, immunologic adjuvant and prevention of diabetes complications. Recently, hypoglycemic and anti-obesity properties of PNS have also been demonstrated. The present review highlights the effects of PNS on glucose production and absorption, and on inflammatory processes that seem to play an important role in the development of diabetes.

Notoginseng Radix et Rhizoma (Sanqi), the underground part of Panax notoginseng (Burk.) F. H. Chen (Araliaceae) is commonly used in Chinese medicine for treatment of haemorrhage, haemostasis, swelling, etc. The aerial part including leaves, flowers and fruits are also applied for similar functions. Triterpenoid saponins are considered to be responsible for the biological activities of Sanqi. Up to date, more than 100 saponins have been isolated from theroots, rhizomes, leaves, flowers and fruits of P. notoginseng. The reported saponins can be classified into protopanaxadiol (PPD), protopanaxatriol (PPT), C17 side-chain varied and other types, according to the skeletons of the aglycons. The present review summarizes the saponins isolated from P. notoginseng and their distribution in different medicinal organs, as well as the pharmacological actions on cardiovascular system.


Rutin (Figure (Figure3B),3B), a glycoside of quercetin, is found in many foods such as red wine, apples and onions. Panchal et al[99] first proved that rutin can decrease adiposity, improve insulin sensitivity, and reduce cardiac remodeling and liver injury in HFD rats[100]. Consistently, in a successive study, rutin effectively inhibited palmitate-induced macrophage activation and reduced liver fat by suppressing transcription of SREBP-1c and CD36 in the liver[101]. Recently, troxerutin was also shown to reduce liver steatosis and improve metabolic syndrome-related pathology in mice fed a high-fat diet, by suppressing oxidative stress-mediated NAD depletion and stimulating fat oxidation[99]. Other flavonoids, including pueraria[102], baicalein[103], luteolin[104], hydroxysafflor yellow A[105], genistein[106,107], silybin[108], isorhamnetin[109], iridin[110], naringin[111], shikonin[112], apigenin[113], kaempferol[114], myricetin[115], and pinocembrin[116] (Figure (Figure3C-P),3C-P), also play significant roles in the treatment of NAFLD.


Curcumin (Figure (Figure3R),3R), responsible for the yellow colour of the plant Curcuma Longa L, is extracted from curry and spice. Its antioxidant properties are widely studied in liver metabolism[132]. Curcumin has also been studied for NASH and metabolic pathologies. Leclercq et al[133] showed that curcumin improves liver injury by inhibiting nuclear factor-kappa B (NF-κB) activation, which in turn inhibits the expression of NF-κB target genes, including intercellular cell adhesion molecule-1, cyclooxygenase-2, and monocyte chemotactic protein 1. Vizzutti et al[134] later extended that curcumin can reduce alpha-smooth muscle actin a level in the NASH mice and can reduce the production of reactive oxygen species and tissue inhibitor of metalloproteinases-1 secreting activated hepatic stellate cells. While some dietary supplements containing curcumin are commercially available, it should be emphasized that case-reports and case series provide insufficient clinical evidence to draw firm conclusions. Polyphenols including techin-3-gallate[135], salvianolic acid B[136], anthocyanidin[137], ellagic acid[138] and cyanidin-3-glucoside[139] (Figure (Figure3S-W)3S-W) also play significant roles in the treatment of NAFLD.

Curcumin alleviates the severity of hepatic inflammation in experimental steatohepatitis induced by the MCD diet, an effect likely to be mediated via inhibition of NF-kB activation and dependent pro-inflammatory genes. The NF-kappaB pathway is one among several possible signalling pathways by which inflammation is recruited in experimental steatohepatitis.


Saponins are glycoside aglycones of three terpenoids or spirostane compounds, mainly found in terrestrial plants[147]. The primary active ingredients in many Chinese traditional herbs, such as Panax ginseng (C. A. Mey.), Polygala tenuifolia (Willd.), Glycyrrhiza uralensis (Fisch), and Platycodon grandiflorus (Jacq.) A. DC., are saponins. Some saponins also have anti-bacterial, anti-pyretic, and anti-cancer activities[148,149].

Dioscin (Figure (Figure4E)4E) is a natural steroid saponin widely found in various herbs[150]. Previous studies have demonstrated that dioscin has anti-tumor[151], anti-hyperlipidemic[152], and anti-fungal activities[153]. Studies have shown that dioscin can gradually reduce the weight, but not suppress appetite or increase physical activity in obese mice. Oral administration of dioscin reduces blood lipid levels, improves fat accumulation in the liver, decreases liver cholesterol and FA and triglyceride deposition through inhibition of FAS, promotes FA beta oxidation, reduces oxidative stress and inflammation, and regulates the MAPK signaling pathway and autophagy[154]. Other saponins such as ginsenoside Rb1[155], ginsenoside Rg1[156] and trillin[157] (Figure (Figure4F-H)4F-H) also play significant roles in the treatment of NAFLD.


Alkaloids are a group of nitrogenous organic compounds present in nature. They are widely found in dicotyledons. They have many pharmacological activities, such as anti-bacterial, anti-inflammatory, analgesic, anti-tumor, and anti-fungal actions[158,159]. A large number of studies have indicated that alkaloids have significant effects on NAFLD.

Berberine (Figure (Figure4I)4I) is isolated from the herb Coptis chinensis Franch. and widely used to treat diarrhea and other inflammatory diseases in China[160]. Recent studies have proved a new therapeutic function of berberine in metabolic disorders, including obesity and diabetes[161,162]. Berberine can be used as a cholesterol lowering drug, through a unique mechanism distinct from statins[163]. These studies suggested a potential therapeutic activity of berberine for NAFLD. Liver gene expression profile analysis showed that high fat diet induced hepatic steatosis in rats led to global changes in gene expression, and treatment with berberine reversed this process. Several modules of berberine-regulated genes, including abundant long non-coding RNAs (lncRNAs), were identified by bioinformatics analysis.

NfKB protein as first responder to harmful toxins – infection – cancer

Nutrigenomics is the idea that studying diet-gene interactions can help identify the positive or detrimental effects of dietary compounds. For example, nutrigenomics can explain why eating rancid or oxidized omega-fats and refined sugar encourages inflammation and cancer growth.

It is important to understand that a diet rich in omega-3 fats can reduce inflammation in cancer. So can healthy omega-6 fats like gamma linoleic acid (GLA), found in evening primrose, black currant seed, and borage oil. GLA inhibits the action of the cancer gene HER-2/neu, which is overexpressed in 30 percent of all breast cancers, making them particularly lethal.

According to Donnie Yance, clinical master herbalist and certified nutritionist, chronic conditions such as cancer and cardiovascular disease have a strong link with chronic inflammation, which promotes the production of free radicals.

The transcription protein Nuclear Factor-kappa Beta (NfKB) is a major inducer of inflammation. In cancer, a mutation in the tumor suppressor gene PTEN (phosphatase and tensin homologue) is the likely driver that activates NfKB.

Some plant-based phytocompounds can enhance PTEN expression or inhibit PTEN mutation, including quercetin, resveratrol, and various isoflavones often referred to as phytoestrogens. An ever-growing body of evidence suggests that the use of these compounds can and should play an important role in cancer prevention and treatment.

NfKB modulation is an important target for cancer prevention and treatment. NfKB can be modulated by:

  • The curcumin in tumeric

  • Stilbenes such as the resveratrol found in grape skins

  • The proathocyanidins in grape seeds

  • Catechins such as EGCG, which is present in green tea

  • The ursolic acid in holy basil, also called Tulsi, and rosemary

NfKB can also be modulated by a number of other plant-based compounds. For more information, please read Donald Yance’s full paper linked below.

Donald “Donnie” Yance is a clinical master herbalist, certified nutritionist and the author of Herbal Medicine Healing and Cancer. He conducts his practice at the Centre for Natural Healing in Ashland, OR utilizing his unique integrative model known as the Eclectic Triphasic Medical System. Donnie is also the founder and president of the Mederi Foundation for professional education and research and Nautra Health Products where he formulates advanced botanical and nutritional products.


About NfKB

NF-κB is important in regulating cellular responses because it belongs to the category of “rapid-acting” primary transcription factors, i.e., transcription factors that are present in cells in an inactive state and do not require new protein synthesis in order to become activated (other members of this family include transcription factors such as c-Jun, STATs, and nuclear hormone receptors). This allows NF-κB to be a first responder to harmful cellular stimuli. Known inducers of NF-κB activity are highly variable and include reactive oxygen species (ROS), tumor necrosis factor alpha (TNFα), interleukin 1-beta (IL-1β), bacterial lipopolysaccharides (LPS), isoproterenol, cocaine, and ionizing radiation.[21]

Receptor activator of NF-κB (RANK), which is a type of TNFR, is a central activator of NF-κB. Osteoprotegerin (OPG), which is a decoy receptor homolog for RANK ligand (RANKL), inhibits RANK by binding to RANKL, and, thus, osteoprotegerin is tightly involved in regulating NF-κB activation.[22]

Many bacterial products and stimulation of a wide variety of cell-surface receptors lead to NF-κB activation and fairly rapid changes in gene expression.[1] The identification of Toll-like receptors (TLRs) as specific pattern recognition molecules and the finding that stimulation of TLRs leads to activation of NF-κB improved our understanding of how different pathogens activate NF-κB. For example, studies have identified TLR4 as the receptor for the LPS component of Gram-negative bacteria.[23] TLRs are key regulators of both innate and adaptive immune responses.

NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) is a protein complex that controls transcription of DNA, cytokine production and cell survival. NF-κB is found in almost all animal cell types and is involved in cellular responses to stimuli such as stress, cytokines, free radicals, heavy metals,ultraviolet irradiation, oxidized LDL, and bacterial or viral antigens.[1][2][3][4][5] NF-κB plays a key role in regulating the immune response to infection (κ light chains are critical components of immunoglobulins). Incorrect regulation of NF-κB has been linked to cancer, inflammatory andautoimmune diseases, septic shock, viral infection, and improper immune development. NF-κB has also been implicated in processes ofsynaptic plasticity and memory.

nFkb.JPG

 

Curcumin/Turmeric for health and happiness by Lisa Cool

Curcumin, found in the yellow Indian spice turmeric, has amazing health benefits, including elevating mood and combatting depressive symptoms as effectively as the prescription drug Prozac, suggests a recent study published in Phytotherapy Research.

Used as an herbal medicine and food for nearly 4,000 years, turmeric is a well-documented treatment for a wide range of disorders, inspiring researchers to dub it “the golden spice of life” in a scientific review. Indeed, over the past 25 years, more than 3,000 papers have explored the savory flavoring’s medicinal properties in lab tests, animal studies, and human trials.

A “safe and effective” herbal treatment for depression

In the new study, researchers conducted a clinical trial that included 60 patients with major depressive disorder (MDD). The patients were randomly divided into three groups, with one receiving 20 mg of fluoxetine (the generic form of Prozac) daily, another getting 500 mg of curcumin twice a day, and the third group receiving both treatments.

Neither the researchers nor the patients knew which treatment they were taking. After six weeks, the curcumin and fluoxetine groups had comparable improvements in mood, based on their score on a standard rating scale for depression that evaluates mood, feelings of guilt, suicidal ideation, insomnia, anxiety and other symptoms. While the group that received both therapies did even better, the difference in depression scores was not statistically significant.

“It is a novel and surprising application for this natural medicine,” study coauthor Dr. Ajay Goel, of the Baylor Research Institute and Charles A. Sammons Cancer Center, said in a statement. He adds curcumin was also used with “excellent results” in an animal study in which it was compared to both fluoxetine and imipramine (an older drug for depression).

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The new study, the researchers added in the statement, “provides the first human clinical indication that curcumin may be used as an effective and safe treatment for patients with MDD without concurrent suicidal ideation or other psychotic disorders.” However, further research, including large clinical studies, is needed to rigorously evaluate if the golden spice is an effective therapy over the long term.

Patients taking antidepressants should not stop or change their treatment without consulting their healthcare provider. Also talk to your doctor before taking any type of supplement to make sure it’s appropriate for you.

Curcumin and its colorful compounds are found in many foods, including mustard, curry powder, some cereals, cheeses, butter, baked goods, sauces, and many other yellow foods. It is on the FDA’s “generally recognized as safe” list as a food ingredient.

Fights Inflammation, Gum Disease and Other Disorders

Studies also show that curcumin has anti-inflammatory and antimicrobial properties. In fact, another new clinical trial suggests that a 1 percent solution of curcumin (in water) works nearly as well as for killing mouth bacteria as a standard dental mouth rinse (0.2 percent chlorhexidine gluconate or CHX) in 23 patients with chronic periodontal (gum) disease.

The patients were randomly assigned to use curcumin or CHX, while a control group used a saltwater rinse for six months. After one month, the curcumin group showed greater reduction in such problems as bleeding gums, redness, amount of dental plaque, and other signs of gum disease. By the 6-month mark, the CHX group had slightly better results on some measures, and similar ones on others.

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An even newer randomized study of 45 patients with the painful and debilitating bowel disorder ulcerative colitis reported that after 8 weeks, 43.4 percent of patients treated with a curcumin preparation called NCB-02 (administered as an enema) achieved remission after eight weeks, compared to only 36.4 percent of patients given a placebo treatment.

The research was published this month in the Journal of Crohn’s and Colitis, with the study authors recommending that the golden spice be investigated as a novel therapy for ulcerative colitis.

Earlier studies and trials suggest that curcumin and turmeric may also be helpful for the following problems, according to the research review cited above:
•Healing peptic ulcers, according to a clinical trial with 45 patients. After 4 weeks of treatment with turmeric capsules (300 mg each, twice a day), the ulcers disappeared in 48 percent of cases, with ulcer-free cases increasing to 76 percent after 12 weeks. Another trial found the spice to be beneficial for people suffering from indigestion or stomach or intestinal ulcers, but not as effective as antacids.
•Fighting respiratory symptoms. In some studies, turmeric oil was helpful in relieving cough, congestion, and asthma.
•Improves wound healing in animal studies.
•May reduce joint pain and inflammation from arthritis.
•Enhances heart health by lowering blood pressure and making cholesterol less likely to clump into artery-clogging plaque, in animal studies.
•Turmeric oil repels mosquitoes.

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Connie Dello Buono

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Curcumin: anti-parasitic, antispasmodic, anti-inflammatory, gastrointestinal effects, inhibits carcinogenesis and cancer growth

• 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].

References
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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