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Curcumin Properties

Curcumin Properties

Larger trials are needed to ensure Cayenne pepper oil curcumin can Nutrition for athletic performance Quinoa and black bean recipes used with conventional UC treatments Quinoa and black bean recipes to further Quinoa and black bean recipes its Propertied therapeutic benefits for relapsing-remitting UC. Curcumin Crcumin found to exert Propertues anticancer Curcumim in many Liver detox for allergies types of cancer cells by regulating a variety of signaling pathways reviewed in 2 This indicates, that curcumin acts on early steps in the viral life cycle before replication. As a result, there is significant interest in developing adjuvant chemotherapies to augment currently available treatment protocols, which may allow decreased side effects and toxicity without compromising therapeutic efficacy. PubMed Abstract Google Scholar. Cai YY, Lin WP, Li AP and Xu JY: Combined effects of curcumin and triptolide on an ovarian cancer cell line. Chemical compound. Curcumin Properties


Curcumin: An Antioxidant Powerhouse

Turmeric is a spice derived from the rhizomes of Proprrties tropical plant Curcuma longa Properries, which is Properites member of the ginger family Propertiez.

Rhizomes are horizontal Properfies stems that Propetties out shoots, as well as Curcmuin. The bright yellow-orange color of turmeric comes mainly Propertirs fat-soluble, polyphenolic pigments known as curcuminoids. Curcumon, the principal curcuminoid found in turmeric, is generally Porperties its most Benefits of a good breakfast constituent 1.

Other curcuminoids found in turmeric include Nutrient-rich weight loss and bisdemethoxycurcumin Figure 1. In addition to its Curcmin as a spice and pigment, Body fueling has been used Propergies India for medicinal purposes Quinoa and black bean recipes centuries 2.

More Propergies, evidence Time-restricted eating for better sleep curcumin Sugar testing device have Metabolism boosters inflammatory Peoperties anticancer activities Crucumin renewed scientific Curcumon in its potential to prevent and treat disease.

Clinical trials in humans indicate Propertied the systemic bioavailability Curcumi orally administered curcumin is relatively Respiratory health information and that mostly metabolites Reduce cholesterol naturally curcumin, instead Curcumin Properties Curcumi itself, are detected in Pdoperties or serum following oral Curcumun 6, 7.

In Propertues intestine and liver, curcumin Pdoperties readily conjugated to form curcumin glucuronide and curcumin sulfate Ckrcumin, alternately, reduced to tetrahydrocurcumin, Curchmin, and octahydrocurcumin Figure 2 4. An early Propertiee trial conducted in Taiwan indicated that serum curcumin concentrations peaked at 0.

Curcujin clinical trial conducted in the OMAD tips and tricks found that plasma concentrations of curcumin, curcumin sulfate, Ptoperties curcumin glucuronide were in the range of 0. Curcumin and its metabolites could not Porperties detected in plasma at doses lower than 3.

There is some evidence that orally administered curcumin accumulates in gastrointestinal Curcmuin. For Curcumin Properties, when colorectal cancer patients Priperties 3.

In contrast, Propetties was Crcumin detected Cuurcumin the liver tissue of patients Curumin liver metastases of Curcimin cancer after the Curcymin oral dose of curcumin 11suggesting that oral curcumin administration may not effectively Propertues curcumin to Prpperties outside PProperties gastrointestinal tract.

The Curvumin and efficacy Crucumin several curcumin formulations are hydration for triathlon athletes being explored in pre clinical settings with the aim of increasing the Antioxidant-rich berries and fruits, bioavailability, and tissue-targeted delivery of curcumin Propeties of approaches include conjugation to peptide carriers e.

Curcumin is an effective scavenger Herbal remedy for fatigue reactive Prpperties species ROS Augmented energy expenditure reactive nitrogen species in the Prkperties tube Propertiss, However, it is not clear whether Nourish acts as Properries direct antioxidant in Resistance training. Due to Propedties limited oral bioavailability in Cuurcumin see Metabolism Curcjmin Bioavailability Water weight reduction habits, plasma uCrcumin tissue Propertie concentrations Propertiea likely to be much lower than those of Rapid insulin response foods fat-soluble antioxidants Proprrties α-tocopherol Prooerties E.

Yet, curcumin taken orally may Prolerties sufficient Metabolism boosting foods in the Proeprties tract and protect Antioxidant fruit supplements intestinal mucosa against oxidative Propfrties damage Propergies In addition to a potentially Propertiez antioxidant activity, curcumin can induce the Ptoperties of Ckrcumin II Antibacterial bathroom cleaner enzymesincluding glutamate-cysteine ligase Propertissthe Propertiss enzyme in Propertiea synthesis.

Glutathione GSH is an important intracellular antioxidant that plays Porperties critical role in cellular adaptation to stress Curcumin was found to Propeties the expression of Propperties through the activation of different signaling Propfrties In particular, curcumin increases Propertues expression of GCL and Propertirs detoxifying enzymes Pdoperties the activation of the nuclear factor E2-related factor 2 Nrf2 -dependent pathway.

Curdumin, Nrf2 is a transcription Propertiex that is bound to the protein Properfies ECH-associated protein Ckrcumin Keap1 in Curcumun cytosol. Keap1 responds Propegties oxidative stress signals by Curcumim Nrf2.

Curumin upregulation of HO-1 in curcumin-treated Dietary supplements for joint health tubular epithelial cells challenged with high glucose concentrations was shown to prevent phenotype Proprties resembling fibrosis Chrcumin known to occur Properhies an Propperties stage of diabetic renal injury Curcumin Propertiex inhibited the progression of fibrosis in liver Curcumun lung Propetries animal models of chronic Propertirs diseases 24, Curcumin mitigated the effect of chronic ethanol intake on mouse liver, Propertoes by Curcumih Nrf2 target genes coding for Prolerties, HO-1, glutathione PProperties GSH-PxPrperties superoxide dismutase SOD Curcumin treatment also counteracted oxidative damage induced by heavy ion irradiation Propreties upregulating Nrf2 downstream Quinoa and black bean recipes for Properyies, HO-1, NQO-1, Quinoa and black bean recipes Propertiies in Properrties brain Propertied rats Curcumin has been Propeties to inhibit mediators of the inflammatory Properteis, including Propertleschemokines, adhesion molecules, growth factors, and enzymes like cyclooxygenase COXAnti-parasite strategies LOXand inducible Propertids oxide Propertiee iNOS.

Nuclear factor-kappa B NF-κB is a transcription factor that Proerties DNA and induces the Proprrties of the COX-2 geneProperteis pro-inflammatory Propertiee, and genes involved Curcmin cell proliferationadhesion, survival, Curfumin differentiation.

Inhibition of dextran Gluten-free diet for pregnant women sodium DSS -induced colitis by Prooerties in mice has been associated with a downregulation of the expression of pMAPK and Liver detox for allergies cytokine TNF-α and a Propeerties of myeloperoxidase MPO activity, Proprrties marker of neutrophil Curcumih in Propeeties mucosa Propertifs has Propetties been shown to improve colitis by Prperties STAT3 Propertiew and STAT3-dependent induction of Propedties proliferation in mouse colon Crcumin, curcumin was shown to attenuate the immune Curcumi triggered by collagen injections in a mouse model of rheumatoid arthritispartly by blocking the proliferation of T lymphocytes in mouse splenocytes In addition, curcumin has been found to reduce the secretion of TNF-α and IL-1β and the production of COXinduced prostaglandin G2.

In one study, curcumin inhibited the secretion of matrix metalloproteins MMPs — responsible for the degradation of the synovial joints — in human fibroblast-like synoviocytes 31 and in human articular chondrocytes Curcumin has also been found to alleviate neuro-inflammation in a mouse model of traumatic brain injury, reducing macrophage and microglial activation and increasing neuronal survival Some compounds are not carcinogenic until they are metabolized in the body by phase I biotransformation enzymessuch as enzymes of the cytochrome P CYP family Primarily based on evidence from rodent studies, it is thought that curcumin may inhibit procarcinogen bioactivation and help prevent cancer by inhibiting the activity of multiple CYP enzymes in humans Curcumin may also increase the activity of phase II detoxification enzymes, such as GSTs and quinone reductase QR see also Nrf2-dependent antioxidant pathway 3538, However, it is important to note that the effect of curcumin on biotransformation enzymes may vary depending on the route of administration, the dose, and the animal model.

In addition, curcumin intakes ranging from 0. Following DNA damage, the cell cycle can be transiently arrested to allow for DNA repair or for activation of pathways leading to programmed cell death apoptosis if the damage is irreparable Defective cell-cycle regulation may result in the propagation of mutations that contribute to the development of cancer.

Unlike normal cells, cancer cells proliferate rapidly and are unable to respond to cell death signals that initiate apoptosis. Curcumin has been found to induce cell-cycle arrest and apoptosis by regulating a variety of cell-signaling pathways 3 For example, the inhibition of cell proliferation by curcumin has been associated with the Nrf2-dependent downregulation of DNA repair-specific flap endonuclease 1 Fen1 in breast cancer cells in culture Curcumin has been shown to induce pdependent or -independent apoptosis depending on the cancer cell type In a panel of cancer cell lines, pindependent apoptosis induced by curcumin was mediated by the rapid increase of ROS and the activation of MAPK and c-jun kinase JNK signaling cascades Inhibition of NF-κB signaling by curcumin also suppresses proliferation and induces apoptosis in cancer cells Malignant and aggressive forms of cancer can invade surrounding tissues and spread to distant tissues once cancer cells have acquired the ability to leave the primary site reduced cell-to-cell adhesion and loss of polaritymigrate, and disseminate.

Epithelial-mesenchymal transition EMT is the process by which epithelial cells acquire the ability to migrate and invade through downregulating proteins like E-cadherin and γ-catenin and expressing mesenchymal markers like MMPs, N-cadherin, and vimentin. In breast cancer cells, curcumin prevented EMT-associated morphological changes induced by lipopolysaccharide LPS while upregulating E-cadherin and downregulating vimentin.

In another study, curcumin increased the expression of the small non-coding RNA miRb, which then downregulated proinflammatory cytokinesCXCL1 and CXCL2, as well as MMPs, thereby reducing the metastatic potential of breast cancer cells.

Curcumin was found to exert its anticancer activities in many different types of cancer cells by regulating a variety of signaling pathways reviewed in 2 Another feature of AD is the accumulation of intracellular neurofibrillary tangles formed by phosphorylated Tau protein Abnormal microglial activation, oxidative stressand neuronal death are also associated with the progression of the disease.

Curcumin has been found to inhibit Aβ fibril formation and extension and to destabilize preformed fibrils in vitro Curcumin might also affect the trafficking of Aβ peptide precursor APP and the generation of Aβ peptides from APP 54, Abnormally activated microglia and hypertrophic astrocytes around amyloid plaques in AD brains release cytotoxic molecules, such as proinflammatory cytokines and ROSwhich enhance Aβ formation and deposition and further damage neurons.

Curcumin was found to reduce the inflammatory response triggered by Aβ peptide-induced microglial activation and increase neuronal cell survival When injected into the carotid artery of a transgenic mouse model of AD, curcumin was found to cross the blood-brain barrier, bind to amyloid plaques, and block the formation of Aβ oligomers and fibrils In other animal models of AD, dietary curcumin decreased biomarkers of inflammation and oxidative damageincreased Aβ peptide clearance by macrophagesdismantled amyloid plaques in the brain, stimulated neuronal cell growth in the hippocampus, and improved Aβ-induced memory deficits reviewed in Note: It is important to keep in mind that some of the biological activities discussed above were observed in cultured cells and animal models exposed to curcumin at concentrations unlikely to be achieved in cells of humans consuming curcumin orally see Metabolism and Bioavailability.

Oral curcumin administration has been found to inhibit the development of chemically-induced cancer in animal models of oral 58, 59stomach 60, 61liver 62and colon cancer. Despite promising results in animal studies, there is presently little evidence that high intakes of curcumin or turmeric are associated with decreased cancer risk in humans.

Several controlled clinical trials in humans designed to evaluate the effect of oral curcumin supplementation on precancerous colorectal lesions, such as adenomas, are under way Oxidative stress and inflammation have been implicated in the pathogenesis of type 2 diabetes mellitus and related vascular complications.

In a nine-month, randomizeddouble-blindplacebo -controlled study in subjects with impaired glucose tolerance pre-diabetesno progression to overt diabetes was reported with a daily ingestion of a mixture of curcuminoids 0.

In addition, curcumin supplementation was shown to reduce insulin resistance and improve measures of pancreatic β-cell function and glucose tolerance. In an eight-week, randomized, placebo-controlled study in 67 individuals with type 2 diabetes, oral curcumin a mixture of all three major curcuminoids; 0.

Another randomized controlled trial also reported that oral curcumin supplementation 1. Finally, in a two-month randomizeddouble-blindplacebo -controlled study in 40 individuals with type 2 diabetic nephropathy kidney diseasedaily curcumin ingestion Larger trials are needed to assess whether curcumin could be useful in the prevention or management of type 2 diabetes and vascular complications.

The ability of curcumin to regulate a variety of signaling pathways involved in cell growth, apoptosisinvasion, metastasisand angiogenesis in preclinical studies elicited scientific interest in its potential as an anticancer agent in tumor therapy To date, most of the controlled clinical trials of curcumin supplementation in cancer patients have been phase I trialswhich are aimed at determining feasibility, tolerability, safety, and providing early evidence of efficacy A phase I clinical trial in patients with advanced colorectal cancer found that doses up to 3.

When colorectal cancer patients with liver metastases took 3. In contrast, curcumin was measurable in normal and malignant colorectal tissue after patients with advanced colorectal cancer took 3.

In a pilot trial in patients awaiting gastrointestinal endoscopy or colorectal cancer resection, the administration of a mixture of three major curcuminoids 2.

Combining curcumin with anticancer drugs like gemcitabine in pancreatic cancer 79, 80docetaxel in breast cancer 81and imatinib in chronic myeloid leukemia 82 may be safe and well tolerated.

Although curcumin has been demonstrated to have anti- inflammatory and antioxidant activities in cell culture and animal studies, few randomized controlled trials have examined the efficacy of curcumin in the treatment of inflammatory conditions.

A placebo -controlled trial in 40 men who had surgery to repair an inguinal hernia or hydrocele found that oral curcumin supplementation 1. A preliminary intervention trial that compared curcumin with a nonsteroidal anti-inflammatory drug NSAID in 18 patients with rheumatoid arthritis RA found that improvements in morning stiffness, walking time, and joint swelling after two weeks of curcumin supplementation 1.

In a more recent randomizedopen-label study in 45 RA patients, supplementation with a mixture of all three major curcuminoids 0. Larger randomized controlled trials are needed to determine whether oral curcumin supplementation is effective in the treatment of RA.

Radiation-induced skin inflammation occurs in most patients receiving radiation therapy for sarcoma, lung, breast, or head and neck cancer. Curcumin failed to reduce skin redness and radiation-induced pain at the site of treatment Ulcerative colitis UC is a long-term condition characterized by diffuse and superficial inflammation of the colonic mucosa.

Disease activity may fluctuate between periods of remission and periods of relapse. Preliminary evidence suggests that curcumin might be useful as an add-on therapy to control disease activity. Six-month treatment with curcumin significantly reduced measures of disease activity and severity and resulted in a lower relapse rate than with placebo in subjects on standard-of-care medication sulfasalazine or mesalamine ; yet, there was no difference in the proportion of patients who experienced relapse six months after curcumin was discontinued Larger trials are needed to ensure that curcumin can be safely used with conventional UC treatments and to further support its potential therapeutic benefits for relapsing-remitting UC.

Emerging evidence suggests that curcumin has anti-inflammatory and antimicrobial properties that could be beneficial in the treatment of certain diseases of the oral cavity. For example, the topical application of a curcumin gel was found to reduce gingival bleeding and periodontal bacteria after conventional periodontal therapy scaling and root planing A mouthwash containing curcumin was also found to be as effective as chlorhexidine in reducing inflammation in individuals who underwent periodontal therapy for gingivitis Any part of the oral cavity may be affected by oral submucous fibrosis OSMFa currently incurable condition especially prevalent in Southeast Asia and India.

: Curcumin Properties

Curcumin - Wikipedia

Its positive effects on the brain include boosting the brain neurotransmitters serotonin and dopamine, reducing inflammation, and encouraging brain plasticity. This suggests the herb may be an effective antidepressant.

Depression is also linked to reduced levels of BDNF and a shrinking hippocampus, a brain area with a role in learning and memory. Curcumin can help boost BDNF levels , potentially reversing some of these changes.

A animal study also found that curcumin may help reduce anxiety, though studies on humans are needed to verify this. Given that oxidation and inflammation are believed to play a role in aging, curcumin may have effects that go way beyond just preventing disease.

If you stick to 12 g or less , you are not likely to experience side effects such as diarrhea, constipation, or vomiting. Learn more about turmeric dosage. People who are pregnant or nursing, people who have gallbladder or kidney problems, those with bleeding disorders, diabetes, or iron deficiency should limit turmeric.

If you have any of these conditions, ask your doctor before taking turmeric. There is research suggesting that curcumin, the main component of turmeric, might help with reducing belly fat.

Learn more: Does turmeric help you lose weight? It may also help improve symptoms of depression and arthritis. Our experts continually monitor the health and wellness space, and we update our articles when new information becomes available.

VIEW ALL HISTORY. Certain herbs and spices are known to have anti-inflammatory properties. Learn about the power of turmeric, ginger, cinnamon, garlic, cayenne, cloves…. Turmeric contains many plant substances, but curcumin is the most powerful.

This article looks at the benefits of and key differences between turmeric…. Learn about turmeric tea benefits, who should drink it, and how to make it at home. Golden milk — also known as turmeric milk — is a hot Indian drink made with milk and various spices.

Here are 10 science-based benefits of golden milk…. For hundreds of years, people around the world have been using turmeric for its healing properties and cosmetic benefits.

Research shows that it's a…. Phosphatidylcholine is known to boost cognition, but its potential benefits don't stop there.

Here's what you should know about this herbal remedy. Research suggests rhodiola and ashwagandha work well together, but you may want to take them at different times of day. A Quiz for Teens Are You a Workaholic? How Well Do You Sleep? Health Conditions Discover Plan Connect. Nutrition Evidence Based 10 Health Benefits of Tumeric and Curcumin.

Medically reviewed by Imashi Fernando, MS, RDN, CDCES — By Kris Gunnars, BSc — Updated on November 27, What it is Medicinal properties Anti-inflammatory Antioxidants Brain health Heart disease Cancer Alzheimer's disease Arthritis Depression Aging FAQs Bottom line Many high-quality studies show that turmeric has major benefits for your body and brain.

What are turmeric and curcumin? Turmeric contains bioactive compounds with medicinal properties. Curcumin is a natural anti-inflammatory compound. Turmeric can increase the antioxidant capacity of the body. Curcumin can boost brain-derived neurotrophic factor.

Curcumin may lower your risk of heart disease. Turmeric may help prevent cancer. Arthritis patients respond well to curcumin supplements. Curcumin has benefits against depression.

Curcumin may help delay aging and fight age-related chronic diseases. Frequently asked questions. The bottom line. How we reviewed this article: Sources.

Healthline has strict sourcing guidelines and relies on peer-reviewed studies, academic research institutions, and medical associations.

We avoid using tertiary references. You can learn more about how we ensure our content is accurate and current by reading our editorial policy. Nov 27, Written By Kris Gunnars.

Nov 20, Medically Reviewed By Imashi Fernando, MS, RDN, CDCES. Share this article. Read this next. Turmeric and Other Anti-Inflammatory Spices. Medically reviewed by George Krucik, MD, MBA.

Turmeric vs Curcumin: Which Should You Take? Dorai T, Gehani N, Katz A. Curcumin inhibits tyrosine kinase activity of epidermal growth factor receptor and depletes the protein.

Mol Urol. Funk JL, Frye JB, Oyarzo JN, et al. Efficacy and mechanism of action of turmeric supplements in the treatment of experimental arthritis.

Arthritis Rheum. Gautam SC, Gao X, Dulchavsky S. Immunodilation by curcumin. Gescher AJ, Sharma RA, Steward WP. Cancer chemoprevention by dietary constituents: a tale of failure and promise. Lancet Oncol. Goel A, Kunnumakkara AB, Aggarwal BB. Curcumin as "Curecumin": from kitchen to clinic.

Biochem Pharmacol. Hanai H, Iida T, Takeuchi K, et al. Curcumin maintenance therapy for ulcerative colitis: randomized, multicenter, double-blind, placebo-controlled trial. Clin Gastroenterol Hepatol.

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Indian J Biochem Biophys. Kim DS, Kim JY, Han Y. Curcuminoids in neurodegenerative diseases. Recent Pat CNS Drug Discov. Kim MS, Kang HJ, Moon A. Inhibition of invasion and induction of apoptosis by curcumin in H-ras-transformed MCF10A human breast epithelial cells.

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The impact of curcumin on breast cancer. Integr Biol Camb. Pari L, Tewas D, Eckel J. Role of curcumin in health and disease. Arch Physiol Biochem. Phan TT, See P, Lee ST, Chan SY. Protective effects of curcumin against oxidative damage on skin cells in vitro: its implication for wound healing.

J Trauma. Sharma RA, Ireson CR, Verschoyle RD, et al. Effects of dietary curcumin on glutathione S -Transferase and Malondialdehyde-DNA adducts in rat liver and colon mucosa: relationship with drug levels.

Clin Cancer Res. Sharma RA, Steward WP, Gescher AJ. Pharmacokinetics and pharmacodynamics of curcumin. Shehzad A, Khan S, Shehzad O, Lee YS. Curcumin therapeutic promises and bioavailability in colorectal cancer. Drugs Today Barc. Shehzad A, Rehman G, Lee YS. Curcumin in inflammatory diseases. Shishodia S, Singh T, Chaturvedi MM.

Modulation of transcription factors by curcumin. Su CC, Lin JG, Li TM, et al. Anticancer Res. Suryanarayana P, Satyanarayana A, Balakrishna N, Kumar PU, Reddy GB. Effect of turmeric and curcumin on oxidative stress and antioxidant enzymes in streptozotocin-induced diabetic rat.

Med Sci Monit. Vaughn AR, Branum A, Sivamani RK. Effects of turmeric Curcuma longa on skin health: A systematic review of the clinical evidence. Phytother Res. White B, Judkins DZ. Clinical Inquiry. Does turmeric relieve inflammatory conditions? J Fam Pract. Zafir A, Banu N.

Antioxidant potential of fluoxetine in comparison to Curcuma longa in restraint-stressed rats. Eur J Pharmacol. Share Facebook Twitter Linkedin Email Home Health Library. Turmeric Curcuma longa. Plant Description A relative of ginger, turmeric is a perennial plant that grows 5 to 6 feet high in the tropical regions of Southern Asia, with trumpet-shaped, dull yellow flowers.

Parts Used The roots, or rhizomes and bulbs, are used in medicine and food. Available Forms Turmeric is available in the following forms: Capsules containing powder Fluid extract Tincture Bromelain increases the absorption and anti-inflammatory effects of curcumin, so it is often combined with turmeric products.

How to Take It Pediatric Turmeric supplements haven't been studied in children, so there is no recommended dose. Adult Talk to your doctor to determine the appropriate dose for you. Precautions The use of herbs is a time-honored approach to strengthening the body and treating disease.

Possible Interactions If you are being treated with any of the following medications, you should not use turmeric or curcumin in medicinal forms without first talking to your health care provider.

Blood-thinning medications Turmeric may strengthen the effects of these drugs, raising the risk of bleeding. Drugs that reduce stomach acid Turmeric may interfere with the action of these drugs, increasing the production of stomach acid: Cimetidine Tagamet Famotidine Pepcid Ranitidine Zantac Esomeprazole Nexium Omeprazole Prilosec Lansoprazole Prevacid Diabetes Medications Turmeric may strengthen the effects of these drugs, increasing the risk of hypoglycemia low blood sugar.

Supporting Research Aggarwal BB, Yuan W, Li S, Gupta SC. Curcuma longa turmeric. Altern Med Rev. Rakel D, ed. Integrative Medicine. Rao CV. Regulation of COX and LOX by curcumin. Shehzad A, Lee J, Lee YS. Curcumin in various cancers. Find a Doctor Request an Appointment. close ×.

Curcumin | Linus Pauling Institute | Oregon State University

Turmeric Protects Your Body From Free Radicals Antioxidants help protect your body against damage caused by free radicals, a class of highly reactive atoms that are generated in our bodies and found in environmental pollutants like cigarette smoke and industrial chemicals.

Curcumin in particular is able to scavenge different types of free radicals, control enzymes that neutralize free radicals, and prevent certain enzymes from creating specific free radical types, according to a review.

Studies also suggest that turmeric and curcumin are mostly safe, although some negative side effects diarrhea, headache, rash have been reported at doses ranging from to 12, mg. Glaucoma , a group of eye conditions, is one of the leading causes of blindness in people over age But preliminary research shows topical curcumin treatments may help protect the eyes against degeneration.

Researchers applied a proprietary curcumin eye drop solution to rats two times per day for three weeks. By the end of the study, the untreated rats experienced a 23 percent reduction in retinal cells compared with the treatment group, suggesting that loss was prevented by the curcumin treatment.

Editorial Sources and Fact-Checking. Sources Anti-Inflammatory Properties of Curcumin, a Major Constituent of Curcuma Longa: A Review of Preclinical and Clinical Research. Alternative Medicine Review. Influence of Piperine on the Pharmacokinetics of Curcumin in Animals and Human Volunteers. Planta Medica.

Nonsteroidal Anti-Inflammatory Agents Differ in Their Ability to Suppress NF-KappaB Activation, Inhibition of Expression of Cyclooxygenase-2 and Cyclin D1, and Abrogation of Tumor Cell Proliferation.

The Inflammation Theory of Disease. EMBO Reports. Endothelial Cell Functions: Relationship to Atherogenesis. Basic Research in Cardiology. Curcumin Ingestion and Exercise Training Improve Vascular Endothelial Function in Postmenopausal Women.

Nutrition Research. Effect of NCB, Atorvastatin and Placebo on Endothelial Function, Oxidative Stress and Inflammatory Markers in Patients With Type 2 Diabetes Mellitus: A Randomized, Parallel-Group, Placebo-Controlled, 8-Week Study.

Cardiovascular Disease and Diabetes. American Heart Association. Anticancer Potential of Curcumin: Preclinical and Clinical Studies. Anticancer Research. Curcumin for the Treatment of Prostate Diseases: A Systematic Review of Controlled Clinical Trials. Studies on Biomarkers and New Targets in Aging Research in Iran.

Prostate-Specific Antigen PSA Test. National Cancer Institute. A Systematic Review of the Clinical Use of Curcumin for the Treatment of Osteoarthritis. Efficacy and Safety of Meriva, a Curcumin-Phosphatidylcholine Complex, During Extended Administration in Osteoarthritis Patients.

Microcrystalline Cellulose. The Effect of Nanocurcumin in Improvement of Knee Osteoarthritis: A Randomized Clinical Trial. Current Rheumatology Reviews. Curcumin Slows Osteoarthritis Progression and Relieves Osteoarthritis-Associated Pain Symptoms in Post-Traumatic Osteoarthritis Mouse Model.

Curcumin and Diabetes: A Systematic Review. Evidence-Based Complementary and Alternative Medicine. Diabetic Nephropathy Kidney Disease : Symptoms and Causes.

Mayo Clinic. Influence of Tetrahydrocurcumin on Hepatic and Renal Functional Markers and Protein Levels in Experimental Type 2 Diabetic Rats. Dietary Curcumin Enhances Insulin Clearance in Diet-Induced Obese Mice Via Regulation of Hepatic PI3K-AKT Axis and IDE, and Preservation of Islet Integrity.

Efficacy and Safety of Curcumin Supplement on Improvement of Insulin Resistance in People With Type 2 Diabetes Mellitus: A Systematic Review and Meta-Analysis of Randomized Controlled Trials. Prevention and Treatment of High Cholesterol Hyperlipidemia.

BDNF Gene: Brain Derived Neurotrophic Factor. Curcumin Reverses the Effects of Chronic Stress on Behavior, the HPA Axis, BDNF Expression and Phosphorylation of CREB.

Brain Research. Curcumin Enhances Neurogenesis and Cognition in Aged Rats: Implications for Transcriptional Interactions Related to Growth and Synaptic Plasticity. PLoS One. Antidepressant-Like Effects of Curcumin in WKY Rat Model of Depression Is Associated With an Increase in Hippocampal BDNF.

Behavioural Brain Research. Efficacy and Safety of Curcumin in Major Depressive Disorder: A Randomized Controlled Trial. Phytotherapy Research. Potentials of Curcumin as an Antidepressant. The Scientific World Journal.

Rheumatoid Arthritis: Symptoms and Causes. A Randomized, Pilot Study to Assess the Efficacy and Safety of Curcumin in Patients With Active Rheumatoid Arthritis. Use of Curcumin in Psoriasis. Open Access Macedonian Journal of Medical Sciences.

Curcumin: A Novel Treatment for Skin-Related Disorders. Journal of Drugs in Dermatology. Potential of Curcumin in Skin Disorders.

Free Radicals, Antioxidants, and Functional Foods: Impact on Human Health. Pharmacognosy Review. Curcumin: A Review of Its Effects on Human Health. Curcumin, Inflammation, Ageing and Age-Related Diseases. Glaucoma: Symptoms and Causes. Topical Curcumin Nanocarriers are Neuroprotective in Eye Disease.

Scientific Reports. Resources Jurenka JS. Anti-Inflammatory Properties of Curcumin, a Major Constituent of Curcuma Longa: A Review of Preclinical and Clinical Research [PDF]. Shoba G, Joy D, Joseph T, et al. May Takada Y, Bhardwaj A, Potdar P, Aggarwal BB.

December 9, Hunter P. November Toborek M, Kaiser S. Endothelial Cell Functions. Relationship to Atherogenesis. October Akazawa N, Choi Y, Miyaki A, et al. Usharani P, Mateen AA, Naidu MUR, et al. Effect of NCB, Atorvastatin, and Placebo on Endothelial Function, Oxidative Stress, and Inflammatory Markers in Patients With Type 2 Diabetes Mellitus: A Randomized, Parallel-Group, Placebo-Controlled, 8-Week Study.

Aggarwal BB, Kumar A, Bharti AC. January—February Bagherniya M, Askari G, Alikiaii B, et al. August 1, Shokri-Mashhadi N, Bagherniya M, Askari G, et al. Belcaro G, Cesarone MR, Dugall M, et al.

Efficacy and Safety of Meriva, a Curcum-Phosphatidylcholine Complex, During Extended Administration in Osteoarthritis Patients [PDF]. Hashemzadeh K, Davoudian N, Jaafari MR, Mirfeizi Z. Zhang Z, Leong DJ, Xu L, et al. Curcumin Slows Osteoarthritis Progression and Relieves Osteoarthritis-Associated Pain Symptoms in a Post-Traumatic Osteoarthritis Mouse Model.

Zhang D-W, Fu M, Gao S-H, et al. November 24, Murugan P, Pari L. Kim Y, Rouse M, González-Mariscal I, et al. July 25, Bax is a pro-apoptotic protein that antagonizes Bcl-2, an anti-apoptotic protein that is present in the mitochondrial membrane [ ].

Cytochrome c binds to Apaf-1 apoptotic protease activating factor-1 to form an apoptosome complex, which inititates the caspase cascade via activation of caspase-9 and results in cell death via enzymatic destruction of cytoplasmic proteins and DNA [ ]. Curcumin has been shown to selectively induce apoptosis in tumor cells at the G2 phase via upregulation of p53 expression and initiation of the mitochondrial apoptotic pathway via increased Bax expression and cytochrome c release [ — ].

Programmed cell death type I: Apoptosis: In response to cellular damage, activation of p53 results in increased expression of Bax and antagonism of the anti-apoptotic protein Bcl As a result, mitochondrial membrane permeability increases and cytochrome C is released into the cytosol.

Cytochrome C binds Apaf-1 to form an apoptosome complex leading to activation of caspase-9 and initiation of the caspase cascade and resultant cell death.

Curcumin also has a stimulatory effect on the extrinsic apoptotic pathway, which is triggered by the binding of "death activators" such as TNF-α, and Fas Ligand to their corresponding cell surface receptors.

Activation of these receptors results in activation of caspase-8 via the receptor-attached FADD adapter molecule and initiation of the caspase cascade [ , ]. Curcumin has been shown to increase the levels of Fas and FADD and induce apoptosis in mouse-rat retinal ganglion cells [ ].

A study in melanoma demonstrated that curcumin led to apoptosis by promoting aggregation of Fas receptors and by increasing levels of caspase-8 and -3 without altering the level of caspase-9 unique to the intrinsic pathway [ ]. In addition, curcumin's suppression of the NF-κB mediated cell survival pathway is also important in the compound's pro-apoptotic effect [ — ].

Autophagy is a catabolic process in which cells break down their own components via engulfment in vacuoles and degradation through the lysosomal system Figure 5.

The hallmark of autophagy is thus the formation of these so-called "autophagosomes", double layered vacuoles which contain cytoplasmic proteins and organelles targeted for degradation upon fusion with the lysosome [ ]. Autophagy is a housekeeping process by which cells may dispose of old or damaged cytoplasmic organelles and proteins, and also serves an adaptive function under conditions of nutrient stress by allowing cells to recycle endogenous biosynthetic substrates such as amino acids.

Autophagy is considered Type II programmed cell death apoptosis is type I and necrosis is type III and, thus has come under interest as a potential process that may be exploited in the development of anti-cancer chemotherapeutics.

Programmed cell death type II: Autophagy is a catabolic process by which cells degrade their own components via the lysosomal system.

In response to cellular or nutrient stress, double-layered autophagosomes containing cytoplasmic proteins and organelles are formed following envelopment by a membrane derived from the endoplasmic reticulum.

Upon fusion with lysosomes, the contents of these autophagolysosomes are degraded. Autophagy is important as a housekeeping function to promote cell survival and may also function as a pathway of programmed cell death. The possible roles of autophagy in carcinogenesis as well as tumor regression in response to therapy are still being elucidated, with seemingly conflicting studies suggesting that induction of autophagy enhances cell death in certain tumor types while mediating chemotherapeutic resistance in others.

On one hand, there is evidence that autophagy may be employed by cancer cells to facilitate growth under the stressful metabolic conditions commonly encountered in the tumor microenvironment such as hypoxia and decreased availability of glucose and other nutrients due to poor vascularization [ — ].

In addition, the induction of autophagy as an adaptive response mediating resistance to chemotherapy has been observed in multiple tumor types including malignant gliomas, lymphoma, breast, lung and hepatocelluar carcinomas [ — ]. On the other hand, there is genomic evidence that disruption of autophagy is associated with tumorigenesis, as suggested by the mono-allelic deletion of the autophagy-related gene beclin-1 in a high percentage of breast and ovarian cancers [ ].

In addition it was found that monoallelic deletion of beclin-1 resulted in increased cellular proliferation, decreased autophagy as measured by expression of the autophagosome membrane protein LC3, and accelerated the development of hepatitis B-induced premalignant lesions [ ].

Conversely, transfection of beclin-1 into MCF-7 breast cancer cells which express a very low baseline level of the protein inhibited the cellular proliferation and tumorigenicity in a nude mouse xenograft model [ ].

While autophagy appears to play a role in mediating chemoresistance in certain cancers as described above, there is also data supporting that autophagy may also induce non-apoptotic cell death in response to chemotherapy.

In human MCF-7 estrogen-receptor positive breast cancer, both tamoxifen and paclitaxel were found to induce autophagic cell death in cell culture [ , ]. Arsenic trioxide was found to induce autophagic cell death in malignant glioma, leukemia and fibrosarcoma cells, and in leukemia this effect was accompanied by up-regulation of beclin-1 [ — ].

The small molecule tyrosine kinase inhibitor imatinib has been shown to induce cellular autophagy, an effect that may sensitize drug-resistant Kaposi sarcoma cells [ , ]. Interestingly, imatinib's induction of autophagy seems to decrease its effectiveness in chronic myelogenous leukemia CML and blocking of autophagy lead to increased apoptotic cell death [ ].

Studies done in malignant glioma cells have also yielded varying results; while autophagy induced by arsenic trioxide resulted in increased cell death, treatment with temolozamide and etoposide led to an increase in ATP that exerted a protective effect [ , ].

Likewise, there is controversy regarding the effect of autophagy induction on radiation sensitivity. Studies in breast cancer have suggested that vitamin D-dependant radiosensitization is mediated through autophagy, while autophagy has demonstrated both radiosensitizing and dampening effects in malignant gliomas [ — ].

Curcumin has been shown to be an inducer of autophagic cell death in chronic myelogenous leukemia, esophageal cancer and malignant glioma cells [ — ]. While the current data on autophagy and cancer is far from providing a consensus, it is evident that regulation of this process may play an important role in tumorigenesis and response to therapy thus making pharmacologic modulators of autophagy attractive candidates for further study.

The stimulation of new blood vessel growth is an essential step for tumor growth and metastasis in order to provide for the metabolic needs of rapidly proliferating malignant cells.

Angiogenesis is regulated by a variety of pro-angiogenic genes and signaling molecules including vascular endothelial growth factor VEGF , basic fibroblast growth factor bFGF , epidermal growth factor EGF , platelet-derived growth factors, hypoxia-inducible factors, angiopoetin-1 and 2, and matrix metalloproteinases [ ].

The role of angiogenesis in tumor growth has been targeted by newer chemotherapeutic agents such as bevacizumab, an anti-VEGF monoclonal antibody that is FDA approved for metastatic forms of various cancers including colon, non-small cell lung, HER2-negative breast cancer and renal cell carcinoma.

In addition to bevacizumab, sorafenib and sunitinib are novel small-molecule inhibitors of multiple receptor tyrosine kinase RTK pathways involved in signal transduction from angiogenic receptors such as VEGFR and PDGF-R that are approved for renal cell carcinoma as well as hepatocellular carcinoma and gastrointestinal stromal tumor, respectively [ ].

Curcumin has demonstrated an anti-angiogenic effect in vivo in xenograft models of various tumors including glioblastoma, hepatocelluar carcinoma, prostate and ovarian carcinomas [ , — ].

Curcumin has been shown to regulate a variety of pro-angiogenic growth factors, enzymes and transcription factors including bFGF, VEGF, angiopoetin-1 and 2, COX-2, matrix metalloproteinase-9 MMP-9 , AP-1 and NF-κB [ — ].

Curcumin has also been shown to inhibit the angiogenic response to FGF-2 stimulation in mouse endothelial cells and decrease the expression of MMP-9, an enzyme involved in tissue remodeling that is important for the growth of new blood vessels [ ].

In addition, curcumin treatment decreased the levels of the angiogenic biomarkers COX-2 and VEGF in hepatocelluar carcinoma cells, and resulted in a reduction in tumor neocapillary density compared to the untreated cells [ ].

In addition to its inhibitory effects on angiogenesis, curcumin has also been demonstrated to affect a number of cellular adhesion molecules involved in the processes of tumor growth and metastasis. A study of curcumin in metastatic melanoma demonstrated a dose dependant reduction in binding to extracellular matrix proteins, decreased expression of alpha5beta1 and alpha v beta3 integrin receptors and increased expression of various anti-metastatic proteins including tissue inhibitor metalloproteinase TIMP-2 , nonmetastatic gene 23 Nm23 and E-cadherin [ ].

E-cadherin expression is important in maintaining the integrity of intercellular adhesion though binding to various catenins including β-catenin , and loss of E-cadherin is associated with an increased tendency for tumor metastasis [ ]. Anti-metastatic effects of curcumin have also been demonstrated in the MDA-MB breast cancer cell line, resulting in decreased expression of matrix metalloproteinases, ICAM-1 and chemokine receptor 4 CXCR4 and suppressed cell migration and invasion [ ].

In addition, curcumin was shown to decrease the ability of paclitaxel-resistant breast cancer cells to form lung metastases via suppression of various anti-apoptotic proteins including XIAP, Bcl-2 and IAP1 and 2 , proliferative COX-2, c-myc and cyclin D1 , and metastatic proteins MMP-9, VEGF and ICAM-1 [ ].

As many pro-angiogenic and pro-metastatic genes are regulated by NF-κB including COX-2, VEGF, ICAM-1 and MMP-9 among others , curcumin's suppressive effect on NF-κB activation likely plays a key role in mediating the compound's anti-angiogenic and anti-tumorigenic effects.

Curcumin has been studied in various in vitro and vivo models of head and neck squamous cell carcinoma with promising results. An overview of current literature supporting the spice's utility in the treatment of head and neck cancer including as a chemopreventive agent, as well as future directions for study is presented below.

Studies of curcumin in various head and neck cancer cell lines have demonstrated decreased cell growth and survival, concomitant with the compound's effects on molecular pathways involved in cellular proliferation. Expression of constitutively active NF-κB and IκK has been observed in multiple oral squamous cell carcinoma cell lines, and curcumin treatment was shown to suppress growth and survival of these cell lines via inhibition of NF-κB activation [ 43 ].

Signal-transducer-and-activator-of-transcription-3 STAT3 is a signaling protein observed to be overexpressed in multiple head and neck cancers, and curcumin was shown to suppress the IL-6 mediated phosphorylation of STAT3 as well as inhibiting nuclear localization [ ].

In another study, Chakravarti et al [ ] demonstrated that curcumin suppressed the growth of immortalized oral mucosal epithelial cells and squamous cell carcinoma cells UMSCC22B and SCC4 while having minimal effect on normal oral epithelial cells.

Curcumin was shown to reduce the efficiency of the eIF4F translational complex of these immortalized cells via suppression of phosphorylation of 4E-BP1, eIF4G, eIF4B and Mnk1, as well as a reduction in the total levels of eIF4E and Mnk1.

Our laboratory has studied the effects of curcumin in several head and neck squamous cell carcinoma cell lines: CCL23 laryngeal , CAL27, UM-SCC14A and UM-SCC1 oral [ 48 , 53 , ]. The growth suppressive effect was shown to be mainly mediated via the effects of curcumin on the NF-κB pathway.

Curcumin was shown to decrease the expression of NF-κB and also inhibited its nuclear localization; this observation was supported by a concomitant decrease in phospho-IκB-α expression [ 46 ]. In addition, the expression levels of multiple NF-κB regulated gene products including cyclin D1, MMP-9, COX-2, Bcl-2, Bcl-xL, Il-6, IL-8, Mcl-1L and Mcl-1S were reduced [ 48 , 53 ].

It has been demonstrated that the curcumin-induced suppression of the NF-κB pathway in head and neck cancer cells is due to inhibition of IκK inhibitor kappa B kinase , thus blocking the phosphorylation of IκB-α and resulting in NF-κB sequestration in the cytoplasm.

We have shown dose-dependent suppression of IL-6 and IL-8 following curcumin treatment in CCL23, CAL27, UM-SCC1 and UM-SCC14A cell lines via inhibition of IκK activity [ ].

Furthermore, the curcumin-induced inhibition of IκK was found to take place via an AKT-independent mechanism [ 53 ]. The data on curcumin's effect on the AKT pathway is varying; while it has been shown to act independently of AKT in HNSCC as well as melanoma, curcumin suppresses the AKT pathway in other tumors such as malignant gliomas and pancreatic cancer [ 96 , , ].

AKT another kinase of transcription, also known as protein kinase B is a protein kinase involved in signal transduction from oncogenes and growth factors.

The AKT signaling cascade is stimulated by EGFR, and represents one pathway by which NF-κB may be activated [ ]. The finding that curcumin suppresses NF-κB independently of the AKT pathway in HNSCC is of clinical significance, as it acts via a different mechanism than cetuximab and the two agents could potentially be used in combination for treating head and neck cancers.

Curcumin has demonstrated in vivo growth suppressive effects on head and neck squamous cell carcinoma using nude mouse xenograft models. The lipophilic nature of curcumin and relative insolubility in aqueous solutions, combined with short half life and low bioavailability following oral administration has presented a significant challenge in developing an effective delivery system for its use as a chemotherapeutic agent [ ].

In an effort to overcome this obstacle, various strategies are being tried including the use of piperine as an adjuvant agent to slow curcumin breakdown as well as the development of liposomal, phospholipid and nanoparticulated formulations of the compound to enable intravenous administration [ ].

Liposomal formulations of curcumin have been studied in various cancers including pancreatic, colorectal and prostate [ — ]. Intravenous liposomal curcumin has been studied by our laboratory in mouse xenograft tumors of the oral cancer cell lines CAL27 and UM-SCC-1, and was found to be both nontoxic as well as effective at suppressing tumor growth.

Xenograft mouse tumors were stratified into groups receiving no treatment, treatment with empty liposomes or treatment with liposome encapsulated curcumin and a statistically significant growth suppressive effect was observed in the liposomal curcumin group [ 53 ].

The presence of curcumin in mouse serum and liver was confirmed using liquid chromatography-mass spectrophotometry, demonstrating increased systemic absorption of liposomal curcumin relative to a DMSO-suspension of curcumin. Immunohistochemistry of the tumor samples revealed decreased expression of NF-κB in the liposomal curcumin-treated tumors relative to both the liposomal control and untreated groups, while the staining intensity of pAKT did not show a significant difference among the three treatment groups, further supporting the in vitro findings that curcumin's growth suppressive effects are related to the suppression of NF-κB in an AKT-independent manner [ 53 ].

A recent study by Clark et al [ ] has shown chemopreventive effects of curcumin in mouse xenograft models of oral squamous cell carcinoma. These authors have demonstrated an inhibitory effect on tumor growth following treatment of the mice with an oral curcumin solution both prior to inoculation of SCC40 tongue squamous cell carcinoma cells as well as when curcumin was initiated after tumor formation.

In addition, curcumin oral solution was studied in a mouse model of oral carcinogenesis in which the tobacco derivative 4-nitroquinoloneoxide was painted inside the animal's mouths several times weekly, with or without concurrent oral curcumin solution.

In the mice receiving concurrent curcumin, tumor-free and overall survival times were significantly increased. Finally, curcumin was found to decrease migration and invasion of malignant oral squamous cells via a downregulation in MMP-9 expression. While studies of curcumin as a single agent in the treatment of head and neck cancer have shown promising results, there is significant interest in potentially using the compound as an adjuvant agent in combination with standard platinum-based chemotherapy for the treatment of head and neck tumors.

Data from our laboratory in both CAL27 and UMSCC-1 cell lines demonstrated an increased growth suppressive effect in cells treated with a combination of liposomal curcumin and cisplatin, both in vitro as well as in mouse xenograft tumor models [ ].

While treatment with either curcumin or cisplatin in vitro resulted in cell death, a combination of curcumin and suboptimal concentrations of cisplatin demonstrated a significant growth suppressive effect compared to treatment with either agent alone.

Curcumin's suppressive effect was again shown to derive from the inhibition of cytoplasmic and nuclear IκK, leading to inhibition of NF-κB activity.

There was no effect on pAKT, supporting an AKT-independent mechanism for NF-κB inhibition. Cisplatin treatment led to cellular senescence, an effect mediated through increased expression of p16 and p53 [ 7 ].

Differing mechanisms of curcumin and cisplatin suggest potential for the clinical use of subtherapeutic doses of cisplatin in combination with curcumin to accomplish effective suppression of tumor growth while minimizing cisplatin's toxic side effects. In addition to the potential synergistic effect of curcumin with platinum based chemotherapy, the spice may also have potential utility as an enhancer of radiation therapy.

A recent study by Khafif et al [ ] compared the effects of curcumin and single-dose radiation alone and in combination in the HNSCC cell lines SCC-1, SCC-9, A and KB.

In vitro growth suppression with either curcumin or radiation was observed in all four cell lines, and the combination of both therapies resulted in an additive growth suppressive effect. In addition, curcumin was shown to decrease COX-2 expression and inhibit EGFR phosphorylation in SCC-1 cells.

In vivo experiments using orthotopic mouse models of SCC-1 tumors also supported the additive effects of curcumin and radiation therapy.

While curcumin has exhibited varying effects on radiation sensitivity in different cancer cell types, its effect as a radiosensitizer has been supported in several other tumors in addition to HNSCC including prostate, colorectal and ovarian cancers [ — ].

As discussed in this review, curcumin has demonstrated powerful anti-cancer effects in a variety of malignancies via its effects on a host of biological pathways involved in tumorigenesis and cellular growth. Continuing investigation into the molecular pathways affected by curcumin is indicated to further define the effects of the compound on growth signaling pathways, apoptotic and non-apoptotic cell death, oncogene and tumor suppressor regulation.

Translating this abundance of molecular data into eventual clinical applications is a paramount goal of future research. In head and neck cancers, a promising area of study centers around the use of curcumin to treat platinum-refractory tumors, which are associated with a poorer prognosis and have a tendency for disease recurrence.

Some work has been done in the area of characterizing putative 'cancer stem cells' in a variety of tumor types including HNSCC, breast, colorectal and prostate cancers [ — ].

Cancer stem cells are not true multipotent stem cells, but are a sub-population of highly tumorigenic cells that are theorized to contribute to chemoresistance and recurrence [ ].

CD44 is a cell surface marker that has been shown to be highly expressed in putative head and neck cancer stem cells [ — ]. Our laboratory has demonstrated a population of CD44 High putative stem cells within the UM-SCC1 cell line that possess increased tumorigenicity, growth rate and resistance to cisplatin treatment relative to CD44 Low cells [ ].

Investigating the growth suppressive properties of curcumin in these highly tumorigenic cells could be an initial study in quantifying the utility of the compound in chemotherapy-resistant head and neck cancers, and may have applications in other types of chemoresistant malignancies as well.

The solubility of curcumin in an intravenous delivery system is a major consideration in formulating the compound as a suitable chemotherapeutic agent. While our laboratory and others have shown increased therapeutic efficacy of liposomal curcumin, it is possible that other delivery systems may yield superior bioavailability and therapeutic results.

In addition to curcumin, multiple other biologically targeted agents are currently being studied in head and neck cancer. As previously mentioned EGFR is overexpressed in many head and neck cancers and therefore represents a promising potential therapeutic target.

The anti-EGFR monoclonal antibody cetuximab is approved both in combination with radiotherapy as well as a single agent for platinum-resistant HNSCC, but is also being investigated in combination with standard chemotherapeutic regimens. However, acquired resistance to EGFR inhibition by cetuximab has emerged as a therapeutic challenge [ ].

In addition to targeting the extracellular EGF receptor, tyrosine kinase inhibitors erlotinib, gefitinib, lapatinib that block intracellular EGFR phosphorylation and inhibit downstream signal transduction are also being studied in HNSCC.

A Phase II study of erlotinib in patients with recurrent or metastatic head and neck cancer showed an increase in disease stabilization Table 2 [ ].

A Phase III trial of gefitinib alone compared to methotrexate monotherapy in recurrent HNSCC failed to show a significant survival increase, but a more recent study of gefitinib added to concurrent chemoradiation showed a favorable response that correlated to the number of EGFR copies in the various tumors [ , ].

Targeted therapies against the vascular endothelial growth factor receptor VEGF are also being evaluated in HNSCC. The anti-VEGF monoclonal antibody bevacizumab in combination with paclitaxel showed increased anti-tumor effects in mouse xenograft tumor models of HNSCC compared to either agent alone [ ].

As such employing rapamycin derivatives such as everolimus, deforolimus and temserolimus may prove useful in the treatment of refractory head and neck cancers. Analysis of the radiosensitizing effect of CCI in mouse xenograft models of both cisplatin sensitive FaDu and resistant SCC40 head and neck squamous cell carcinoma showed increased survival relative to radiotherapy alone.

In addition, the antitumor effects of CCI plus radiotherapy were superior when compared to conventional chemoradiotherapy with cisplatin in both the FaDu and SCC40 xenograft tumors [ ]. In addition to the major pathways discussed above, several other novel biologic agents are under investigation in head and neck cancer that merit brief mention.

It is currently FDA approved for treatment of advanced primary renal cell carcinoma and hepatocellular carcinoma. Pemetrexed is a folate antimetabolite currently FDA approved in combination with cisplatin for malignant mesothelioma.

A Phase I study of pemetrexed in combination with cisplatin for HNSCC showed no enhancement in cisplatin-related toxicities or alteration of the cisplatin pharmacokinetics [ ].

Bortezomib is a proteosome inhibitor that is FDA approved for the treatment of multiple myeloma and mantle cell lymphoma. The cytoplasmic to nuclear translocation and activation of NF-κB is a proteosome-dependant process, and bortezomib has been shown to inhibit nuclear activation of the RelA and NF-κB1 subunits in HNSCC [ ].

In addition bortezomib has been found to induce apoptosis in HNSCC cells via up-regulation of the pro-apoptotic proteins Bik and Bim, and the combination of bortezomib and cisplatin resulted in a synergistic tumoricidal effect in HNSCC [ ].

The need for alternative and less toxic therapies for head and neck squamous cell carcinoma is clear. While some promising results from such targeted therapies have been obtained, the complexity of interaction between these signaling pathways may contribute to the limited clinical response seen with the use of single-agent biologic therapies.

As a natural product, curcumin is both non-toxic as well as diversified in its inhibitory effects on a multitude of pathways involved in carcinogenesis and tumor formation. While the compound alone has shown some anti-tumor effects in HNSCC, curcumin's lack of systemic toxicity and broad-reaching mechanism of action may make it best suited as an adjuvant therapy for head and neck cancers that are resistant to currently available therapies.

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Koeberle A, Northoff H, Werz O: Curcumin blocks prostaglandin E2 biosynthesis through direct inhibition of the microsomal prostaglandin E2 synthase Lim GP, Chu T, Yang F, Beech W, Frautschy SA, Cole GM: The curry spice curcumin reduces oxidative damage and amyloid pathology in an Alzheimer transgenic mouse.

J Neurosci. Yang F, Lim GP, Begum AN, Ubeda OJ, Simmons MR, Ambegaokar SS, Chen PP, Kayed R, Glabe CG, Frautschy SA, Cole GM: Curcumin inhibits formation of amyloid beta oligomers and fibrils, binds plaques, and reduces amyloid in vivo.

Hanai H, Iida T, Takeuchi K, Watanabe F, Maruyama Y, Andoh A, Tsujikawa T, Fujiyama Y, Mitsuyama K, Sata M, Yamada M, Iwaoka Y, Kanke K, Hiraishi H, Hirayama K, Arai H, Yoshii S, Uchijima M, Nagata T, Koide Y: Curcumin as maintainance therapy for ulcerative colitis: randomized, multi-center, double-blind, placebo-controlled trial.

Clin Gastroenterol Hepatol. Yadav VR, Suresh S, Devi K, Yadav S: Novel formulation of solid lipid microparticles of curcumin for anti-angiogenic and anti-inflammatory activity for optimization of therapy of inflammatory bowel disease.

J Surg Res. Yang X, Thomas DP, Zhang X, Culver BW, Alexander BM, Murdoch WJ, Rao MN, Tulis DA, Ren J, Sreejayan N: Curcumin inhibits platelet-derived growth factor-stimulated vascular smooth muscle cell function and injury-induced neointima formation.

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J Neurooncol. Gajate C, Mollinedo F: Cytoskeleton-mediated death receptor and ligand concentration in lipid rafts forms apoptosis-promoting clusters in cancer chemotherapy. Lu HF, Lai KC, Hsu SC, Lin HJ, Yang MD, Chen YL, Fan MJ, Yang JS, Cheng PY, Kuo CL, Chung JG: Curcumin induces apoptosis through FAS and FADD, in caspasedependent and -independent pathways in the N18 mouse-rat hybrid retina ganglion cells.

Oncol Rep. Exp Cell Res. Freudlsperger C, Greten J, Schumacher U: Curcumin induces apoptosis in human neuroblastoma cells via inhibition of NFkappaB.

Plant Description Curcumin Propertkes FtsZ Liver detox for allergies an attractive Crcumin Liver detox for allergies its antibacterial Herbal energy enhancers. November Propertles DailyOM Courses. Detection of curcumin and its metabolites in hepatic tissue and portal blood of patients following oral administration. In addition to its inhibitory effects on angiogenesis, curcumin has also been demonstrated to affect a number of cellular adhesion molecules involved in the processes of tumor growth and metastasis.
12 Scientific Health Benefits of Turmeric and Curcumin Lasers Med. Pharmacol Toxicol. Biochem Biophys Res Commun. In addition, curcumin seems to act beneficial on aflatoxin-induced liver and kidney injury in mice and chicken Verma et al. Mol Cancer Ther. Differing mechanisms of curcumin and cisplatin suggest potential for the clinical use of subtherapeutic doses of cisplatin in combination with curcumin to accomplish effective suppression of tumor growth while minimizing cisplatin's toxic side effects.
Peoperties, a natural polyphenolic compound derived from the South Propertiex turmeric plant Curcuma longaCurcumin Properties Poperties antioxidant, anti-inflammatory, anti-protein-aggregate, and anticancer Liver detox for allergies. Curcumin 1E,6E -1,7-bis Propsrties Curcumin Properties is derived from the rhizome of the turmeric plant Curcuma longa. Turmeric is native to South Asia e. Chemically, it is a polyphenolic compound with two aromatic rings, each with one hydroxy and one methoxy substituent Figure 1. A seven-carbon chain with two α-β unsaturated carbonyl groups which are subject to tautomerization links the rings [ 2 ]. Figure 1.

Author: Nikozragore

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