Life Extension Magazine®

Quercetin’s Unique Protective Mechanisms

People with high intakes of quercetin have significantly lower risk for cardiovascular diseases. Quercetin provides multimodal cardiac protection such as triggering reverse cholesterol transport and improving after-meal endothelial function by 31.4%.

Scientifically reviewed by: Dr. Gary Gonzalez, MD, in August 2023. Written by: Michael Enders.

Quercetin’s Unique Protective Mechanisms  

In our quest to identify cutting-edge therapies to protect against age-related disorders, we sometimes overlook the basics.

Found in certain fruits and vegetables, quercetin has been studied for decades and evidence supporting its biological properties is substantial.

Recent lab and human studies are confirming that quercetin can prevent many of the underlying factors that are destructive to our health. These deleterious biological events are often unnoticed by medical doctors until they manifest as major diseases.

Quercetin fits nicely into a broad-based anti-aging strategy and has long been included in nutrient formulas used by health-conscious individuals.

Protecting Hardworking Heart Muscle

People with high intakes of dietary flavonols and flavones such as quercetin have a demonstrably lower risk for cardiovascular diseases.1,2 Exciting new research suggests that a big part of the reason for this protection is quercetin’s effects on mitochondria.

Proof of the impact of quercetin’s mitochondrial “boost” can be seen in a pair of animal and human exercise studies. Untrained mice supplemented with quercetin for seven days increased both their maximal endurance capacity on a treadmill and their voluntary use of the treadmill, while biopsies showed formation of new mitochondria in their muscles and brains.3

In the companion human trial, untrained volunteers took 500 mg/day of quercetin, or placebo, for seven days, with their exercise performance measured before and after the trial period.4 Subjects taking quercetin modestly increased their oxygen consumption by 3.9%, but increased their riding time to fatigue by 13.2%, entirely without additional training!

In a similar trial, untrained young men who took 1,000 mg/day of quercetin for two weeks also increased the distance they could run on a treadmill by 2.9%, while placebo subjects lost 1.2%; muscle mitochondrial numbers grew by 4.1% in supplemented subjects, while falling 6% in placebo recipients.5

Plaque Regression

Plaque Regression  

Quercetin has been analyzed for its ability to counteract atherosclerosis—the gradual blockage of blood flow through arteries. Atherosclerotic plaques are a major cause of heart attack and stroke, two of the top killers of Americans.

In a study of rabbits fed a high-cholesterol diet, quercetin prevented the oxidative and inflammatory effects of the diet on arterial walls, as expected. But it also promoted regression of atherosclerotic plaque, a direct effect of its inhibition of inflammatory enzymes such as COX and 5-LOX (these enzymes produce pro-inflammatory molecules called prostaglandins and leukotrienes).6

This plaque regression is likely driven by a recently discovered property of quercetin. Scientists found that quercetin triggers reverse cholesterol transport, which is the removal of cholesterol from the arterial wall by HDL for transport to the liver for safe disposal.7-9

Quercetin has additional benefits for the endothelial cells lining the blood vessels that normally control blood flow and pressure. Quercetin restores normal production of the relaxation-signaling molecule nitric oxide, and has been shown to produce relaxation of major arteries to promote improved blood flow.10-12 This played out in an impressive fashion in a human study showing that a quercetin-containing food improved after-meal endothelial function by 31.4%.13

New data on quercetin’s many cardiovascular benefits are being published regularly. Here are just a few highlights from the recent literature:

  • Quercetin counteracts the development of tolerance to nitroglycerin and related drugs used in treatment of angina.14
  • Quercetin reduces abnormal heart rhythms in patients with ischemic heart disease who were already on standard medical therapy.15
  • Quercetin reduces the incidence of abdominal aortic aneurysms in animal models; these deadly defects in the wall of the aorta can lead to sudden death.16
  • Quercetin helps to slow platelet aggregation, which can lead to blood clots that produce heart attacks and strokes.17,18
What You Need To Know
Quercetin Can Restore and Refurbish Mitochondria

Quercetin Can Restore and Refurbish Mitochondria

  • Studies show that quercetin triggers reverse cholesterol transport, which results in the removal of cholesterol from the arterial wall by HDL for transport to the liver for safe disposal.
  • Excitingly, quercetin has been found to activate the brain’s powerful natural antioxidant defense system (called Nrf2) that upgrades cellular defenses such as glutathione and prevents brain cell death.
  • As a neuroprotective agent, quercetin protects brain cells against excitotoxicity, the damage done by repeated excitatory electrical impulses observed in Alzheimer’s and other neurodegenerative diseases.
  • Quercetin, found in onions and apples, has now been shown to preserve mitochondria in the heart, brain, liver, and skeletal muscles.
  • Quercetin boosts cardiovascular function, muscular endurance and performance, protects against loss of brain cells, corrects blood glucose and lipid abnormalities in metabolic syndrome, and shows evidence of anticancer and bone health-promoting properties.

Potent Neuroprotection

Like the heart, the human brain is a major consumer of energy. That means it depends heavily upon its mitochondria to deliver the power needed for normal thought, memory, and cognition. Aging reduces mitochondrial function in the brain, mainly as a result of the strong oxidant impact of electrical and chemical activity.19

Quercetin is showing real promise as a neuroprotective nutrient. Studies show that quercetin protects brain cells against excitotoxicity, the damage done by repeated excitatory electrical impulses observed in Alzheimer’s and other neurodegenerative diseases.20-23 Acting through its antioxidant mechanisms, quercetin may reduce toxicity of the dangerous and abnormal amyloid-beta proteins that accumulate in the brain, eventually producing symptoms of memory loss and dementia.24 In fact, quercetin has now been found to prevent brain cell death in animal models of Parkinson’s disease.25

Excitingly, quercetin has been found to activate the brain’s powerful natural antioxidant defense system (called Nrf2) that upgrades cellular defenses such as glutathione and prevents brain cell death.26 Quercetin also increases brain mitochondrial expression of the protective paraoxonase 2 (PON2), which scavenges the free radicals that break down mitochondrial membranes and cause them to lose their electrical potential.27-29

Chronic oxidation leads to chronic inflammation in the brain as it does in the rest of the body, eventually producing changes that can lead to both Alzheimer’s and Parkinson’s diseases.30 Quercetin is among the nutrient molecules capable of preserving vital brain cell function in the face of those changes, limiting the cell death that produces neurodegenerative diseases.31

Obesity And Metabolic Syndrome

Obesity is best thought of in relation to other metabolic disturbances, such as blood lipid abnormalities, elevated blood sugar, insulin resistance, and hypertension. Together, these problems define metabolic syndrome, which is strongly associated with poor health outcomes and sudden death.32,33 A prospective study assessing the mortality status of 6,678 healthy middle-aged men concluded that metabolic syndrome increased the risk of sudden death from heart attack by 68%.33

It is widely recognized that plant flavonoids, especially quercetin, can play important roles in fighting individual components of metabolic syndrome, and may work to reduce the impact of the syndrome as a whole.34,35 In a laboratory animal model, quercetin completely abolished glucose-induced life span reduction by enhancing natural cellular “clean-up” mechanisms that prevented loss of function.36

Lab studies show that quercetin is effective at suppressing fat accumulation in the liver,37 leading to a reduction in fat-induced inflammation triggered by high levels of leptin, the hormone produced in excess in fat tissue deposits.38-41 An eight-week study demonstrated that quercetin-rich onion skin extracts led to reduced internal fat accumulation while increasing levels of the hormone adiponectin, thus improving insulin sensitivity and promoting weight loss.42

Increased amounts of fat tissue lead directly to insulin resistance, which produces high blood sugar while at the same time starving cells of the glucose they need for normal function.43 In fact, even mild elevations of blood sugar, over a lifetime, can accelerate aging.36 In rats fed a high-fat, high-sugar diet, quercetin reduced blood sugar and insulin release, improving insulin resistance.44 Other studies show that quercetin-supplemented rats fed a high-fat, high-carbohydrate diet had less abdominal fat, lower blood pressure, and reduced heart and liver fat accumulations, likely due to antioxidant and anti-inflammatory mechanisms.32 Similar findings were made in diabetic and insulin-resistant rats.45

But these exciting results are not limited to lab and animal studies. In a group of overweight and obese adults with early metabolic syndrome, just 150 mg of quercetin daily reduced blood pressure and levels of oxidized LDL cholesterol, two major components of metabolic syndrome.46 Another human study found that the same dose of quercetin (150 mg/day) for eight weeks decreased waist circumference and after-meal systolic blood pressure, while also lowering after-meal triglyceride levels in a group of otherwise healthy men.35 Another study showed women with type II diabetes reduced systolic blood pressure nearly nine points after taking quercetin.47

In other words, quercetin supplementation in animal and now in human studies proved capable of reversing the major components of metabolic syndrome.

Cancer Protection From Quercetin

Cancer Protection From Quercetin  

Quercetin has been shown to possess numerous anticancer properties, including the ability to interrupt the rapid cell proliferation cycle in growing cancers, and to induce apoptosis, the programmed cell death that cancer cells have lost.48,49 Quercetin’s actions appear to be cancer type- and site-specific, with its most aggressive action on the most aggressive and rapidly growing cancers of the blood (leukemia), brain, lung, uterus, and skin (melanoma).50

Additional data suggest that quercetin is highly effective in preventing the division of colon cancer cells as well.51 Indeed, one small human study has already shown that the combination of quercetin with curcumin, another potent anti-inflammatory nutrient, can slow the growth of precancerous colonic polyps in patients with familial polyposis, a condition always associated with colorectal cancers.52

Estrogen receptors present on the surface of cells can serve as growth stimulators in many cancer types, including lung cancer.53 A unique property of quercetin is its ability to modulate the activity of estrogen receptors,54 and in a lab study, this attribute was shown to reduce the proliferation of lung cancer cells.55 It was also demonstrated that quercetin binds to estrogen receptors just as tightly as tamoxifen, the drug most commonly used in breast cancer therapy.55 As a result, quercetin effectively inhibited proliferation of dangerous drug-resistant breast cancer cells, while also preventing their accumulation into lump-like clusters capable of growth and invasion.56

Quercetin Fights Mitochondrial Threats To Bone And Joint Health

Quercetin Fights Mitochondrial Threats To Bone And Joint Health  

Quercetin has powerful bone health-promoting effects, some of which were superior to the prescription anti-osteoporosis drug alendronate in preclinical research. Unlike such drugs, quercetin promotes new bone formation, rather than simply slowing bone degradation.57-60 This is important because alendronate and similar drugs act by essentially inhibiting the bone-resorbing cells61 in the hope that the bone-forming cells that remain intact will predominate and keep bones strong. Quercetin, by contrast, works by stimulating new bone production by bone-forming cells, allowing bones to retain their normal responses to physical stress.62

“Secondary” osteoporosis and osteopenia (a condition where bone mineral density is lower than normal) can occur with certain diseases and drug treatments, most commonly chronic steroid use. Lab studies show that both quercetin and alendronate could completely reverse steroid-induced osteoporosis, but quercetin also stimulated new bone formation in rat femurs by up to 36%, while alendronate did not.59 Very similar results were shown in animals with steroid-induced osteoporosis and osteopenia secondary to diabetes, both of which commonly cause bone loss.58,59

In the management of arthritis, quercetin has demonstrated superior anti-inflammatory properties. When a group of flavonoids was studied, quercetin showed the strongest specific inhibitory effects on the pro-inflammatory enzymes COX-1 and 15-LOX, both of which produce powerful pro-inflammatory signaling molecules in arthritis.63 Recent studies suggest that quercetin may also reduce accumulation of stiff, fibrous tissue in inflamed joints, potentially improving their function.64,65

Quercetin may also be effective in ameliorating the intensely painful arthritis caused by gout, in which crystals of uric acid accumulate in the joint and induce vigorous inflammation.65 Animals with gouty arthritis showed reduced joint swelling, reduced white blood cell infiltration, lower oxidant levels, and lower levels of inflammatory cytokines following supplementation with quercetin.66

Human studies of quercetin in osteoarthritis are encouraging, especially given the lack of any known drug that can effectively modify or slow the disease’s progress. Added to a standard joint supplement containing glucosamine and chondroitin, 45 mg/day of quercetin for 12 or 16 weeks significantly improved joint pain and function scores compared with placebo, while laboratory markers of new collagen formation (important in preserving joint function) were increased.67,68


Studies show that quercetin preserves and improves cardiovascular health, slows neurodegeneration, and fights metabolic syndrome. Moreover, quercetin may offer protection against cancer, osteoporosis, and osteoarthritis through its multiple beneficial mechanisms.

The beneficial effects of whole fruits and vegetables in the human diet may be partially explained by the quercetin they contain. Those who don’t consume enough healthy fruits and vegetables can obtain this multi-faceted polyphenol (quercetin) in low-cost supplements.

If you have any questions on the scientific content of this article, please call a Life Extension® Health Advisor at 1-866-864-3027.


  1. Janssen K, Mensink RP, Cox FJ, et al. Effects of the flavonoids quercetin and apigenin on hemostasis in healthy volunteers: results from an in vitro and a dietary supplement study. Am J Clin Nutr. 1998 Feb;67(2):255-62.
  2. Scoditti E, Calabriso N, Massaro M, et al. Mediterranean diet polyphenols reduce inflammatory angiogenesis through MMP-9 and COX-2 inhibition in human vascular endothelial cells: a potentially protective mechanism in atherosclerotic vascular disease and cancer. Arch Biochem Biophys. 2012 Nov 15;527(2):81-9.
  3. Davis JM, Murphy EA, Carmichael MD, Davis B. Quercetin increases brain and muscle mitochondrial biogenesis and exercise tolerance. Am J Physiol Regul Integr Comp Physiol. 2009 Apr;296(4):R1071-7.
  4. Davis JM, Carlstedt CJ, Chen S, Carmichael MD, Murphy EA. The dietary flavonoid quercetin increases VO(2max) and endurance capacity. Int J Sport Nutr Exerc Metab. 2010 Feb;20(1):56-62.
  5. Nieman DC, Williams AS, Shanely RA, et al. Quercetin’s influence on exercise performance and muscle mitochondrial biogenesis. Med Sci Sports Exerc. 2010 Feb;42(2):338-45.
  6. Bhaskar S, Kumar KS, Krishnan K, Antony H. Quercetin alleviates hypercholesterolemic diet induced inflammation during progression and regression of atherosclerosis in rabbits. Nutrition. 2013 Jan;29(1):219-29.
  7. Ohara K, Wakabayashi H, Taniguchi Y, Shindo K, Yajima H, Yoshida A. Quercetin-3-O-glucuronide induces ABCA1 expression by LXRalpha activation in murine macrophages. Biochem Biophys Res Commun. 2013 Nov 29;441(4):929-34.
  8. Lee SM, Moon J, Cho Y, Chung JH, Shin MJ. Quercetin up-regulates expressions of peroxisome proliferator-activated receptor gamma, liver X receptor alpha, and ATP binding cassette transporter A1 genes and increases cholesterol efflux in human macrophage cell line. Nutr Res. 2013 Feb;33(2):136-43.
  9. Derlindati E, Dall’Asta M, Ardigo D, et al. Quercetin-3-O-glucuronide affects the gene expression profile of M1 and M2a human macrophages exhibiting anti-inflammatory effects. Food Funct. 2012 Nov;3(11):1144-52.
  10. Shen Y, Ward NC, Hodgson JM, et al. Dietary quercetin attenuates oxidant-induced endothelial dysfunction and atherosclerosis in apolipoprotein E knockout mice fed a high-fat diet: A critical role for heme oxygenase-1. Free Radic Biol Med. 2013 Dec;65:908-15.
  11. Fitzpatrick DF, Hirschfield SL, Coffey RG. Endothelium-dependent vasorelaxing activity of wine and other grape products. Am J Physiol. 1993;265:H774-8.
  12. Chen CK, Pace-Asciak CR. Vasorelaxing activity of resveratrol and quercetin in isolated rat aorta. Gen Pharmacol. 1996;27:363-6.
  13. Nakayama H, Tsuge N, Sawada H, Higashi Y. Chronic intake of onion extract containing quercetin improved postprandial endothelial dysfunction in healthy men. J Am Coll Nutr. 2013;32(3):160-4.
  14. Durante M, Sgaragli G, Biasutto L, Mattarei A, Fusi F. Quercetin mitochondriotropic derivatives antagonize nitrate tolerance and endothelial dysfunction of isolated rat aorta rings. Planta Med. 2013 Apr;79(6):465-7.
  15. Malishevskaya I, Ilashchuk T, Okipnyak I. Therapeutic efficacy of quercetin in patients with is ischemic heart disease with underlying metabolic syndrome. Georgian Med News. 2013 Dec;(225):67-71.
  16. Wang L, Cheng X, Li H, et al. Quercetin reduces oxidative stress and inhibits activation of cJun Nterminal kinase/activator protein1 signaling in an experimental mouse model of abdominal aortic aneurysm. Mol Med Rep. 2014 Feb;9(2):435-42.
  17. Wright B, Moraes LA, Kemp CF, et al. A structural basis for the inhibition of collagen-stimulated platelet function by quercetin and structurally related flavonoids. Br J Pharmacol. 2010 Mar;159(6):1312-25.
  18. Wright B, Spencer JP, Lovegrove JA, Gibbins JM. Flavonoid inhibitory pharmacodynamics on platelet function in physiological environments. Food Funct. 2013 Dec;4(12):1803-10.
  19. Dorszewska J. Cell biology of normal brain aging: synaptic plasticity-cell death. Aging Clin Exp Res. 2013 Apr;25(1):25-34.
  20. Hynd MR, Scott HL, Dodd PR. Glutamate-mediated excitotoxicity and neurodegeneration in Alzheimer’s disease. Neurochem Int. 2004 Oct;45(5):583-95.
  21. Silva B, Oliveira PJ, Dias A, Malva JO. Quercetin, kaempferol and biapigenin from Hypericum perforatum are neuroprotective against excitotoxic insults. Neurotox Res. 2008 May-Jun;13(3-4):265-79.
  22. Yang EJ, Kim GS, Kim JA, Song KS. Protective effects of onion-derived quercetin on glutamate-mediated hippocampal neuronal cell death. Pharmacogn Mag. 2013 Oct;9(36):302-8.
  23. Dong XX, Wang Y, Qin ZH. Molecular mechanisms of excitotoxicity and their relevance to pathogenesis of neurodegenerative diseases. Acta Pharmacologica Sinica. 2009;30(4):379-87.
  24. Shi C, Zhao L, Zhu B, et al. Protective effects of Ginkgo biloba extract (EGb761) and its constituents quercetin and ginkgolide B against beta-amyloid peptide-induced toxicity in SH-SY5Y cells. Chem Biol Interact. 2009 Sep 14;181(1):115-23.
  25. Karuppagounder SS, Madathil SK, Pandey M, Haobam R, Rajamma U, Mohanakumar KP. Quercetin up-regulates mitochondrial complex-I activity to protect against programmed cell death in rotenone model of Parkinson’s disease in rats. Neuroscience. 2013 Apr 16;236:136-48.
  26. Arredondo F, Echeverry C, Abin-Carriquiry JA, et al. After cellular internalization, quercetin causes Nrf2 nuclear translocation, increases glutathione levels, and prevents neuronal death against an oxidative insult. Free Radic Biol Med. 2010 Sep 1;49(5):738-47.
  27. Costa LG, de Laat R, Dao K, Pellacani C, Cole TB, Furlong CE. Paraoxonase-2 (PON2) in brain and its potential role in neuro-protection. Neurotoxicology. 2013 Sep 4.
  28. Costa LG, Tait L, de Laat R, et al. Modulation of paraoxonase 2 (PON2) in mouse brain by the polyphenol quercetin: a mechanism of neuroprotection? Neurochem Res. 2013 Sep;38(9):1809-18.
  29. Navarro A, Boveris A. The mitochondrial energy transduction system and the aging process. Am J Physiol Cell Physiol. 2007;292:C670–86.
  30. Wenk GL, McGann-Gramling K, Hauss-Wegrzyniak B, et al. Attenuation of chronic neuroinflammation by a nitric oxide-releasing derivative of the antioxidant ferulic acid. J Neurochem. 2004 Apr;89(2):484-93.
  31. Bournival J, Plouffe M, Renaud J, Provencher C, Martinoli MG. Quercetin and sesamin protect dopaminergic cells from MPP+-induced neuroinflammation in a microglial (N9)-neuronal (PC12) coculture system. Oxid Med Cell Longev. 2012;2012:921941.
  32. Panchal SK, Poudyal H, Brown L. Quercetin ameliorates cardiovascular, hepatic, and metabolic changes in diet-induced metabolic syndrome in rats. J Nutr. 2012 Jun;142(6):1026-32.
  33. Empana JP, Duciemetiere P, Balkau B, Jouven X. Contribution of the metabolic syndrome to sudden death risk in asymptomatic men: the Paris Prospective Study I. Eur Heart J. 2007; 28(9): 1149-54.
  34. Hurt RT, Wilson T. Geriatric obesity: evaluating the evidence for the use of flavonoids to promote weight loss. J Nutr Gerontol Geriatr. 2012;31(3):269-89.
  35. Pfeuffer M, Auinger A, Bley U, et al. Effect of quercetin on traits of the metabolic syndrome, endothelial function and inflammation in men with different APOE isoforms. Nutr Metab Cardiovasc Dis. 2013 May;23(5):403-9.
  36. Fitzenberger E, Deusing DJ, Marx C, Boll M, Luersen K, Wenzel U. The polyphenol quercetin protects the mev-1 mutant of Caenorhabditis elegans from glucose-induced reduction of survival under heat-stress depending on SIR-2.1, DAF-12, and proteasomal activity. Mol Nutr Food Res. 2014 May;58(5):984-94.
  37. Wang W, Wang C, Ding XQ, et al. Quercetin and allopurinol reduce liver thioredoxin-interacting protein to alleviate inflammation and lipid accumulation in diabetic rats. Br J Pharmacol. 2013 Jul;169(6):1352-71.
  38. Indra MR, Karyono S, Ratnawati R, Malik SG. Quercetin suppresses inflammation by reducing ERK1/2 phosphorylation and NF kappa B activation in Leptin-induced Human Umbilical Vein Endothelial Cells (HUVECs). BMC Res Notes. 2013 Jul 16;6(1):275.
  39. Jung CH, Cho I, Ahn J, Jeon TI, Ha TY. Quercetin reduces high-fat diet-induced fat accumulation in the liver by regulating lipid metabolism genes. Phytother Res. 2013 Jan;27(1):139-43.
  40. Kobori M, Masumoto S, Akimoto Y, Oike H. Chronic dietary intake of quercetin alleviates hepatic fat accumulation associated with consumption of a Western-style diet in C57/BL6J mice. Mol Nutr Food Res. 2011 Apr;55(4):530-40.
  41. Noh HJ, Kim CS, Kang JH, et al. Quercetin Suppresses MIP-1alpha-Induced Adipose Inflammation by Downregulating Its Receptors CCR1/CCR5 and Inhibiting Inflammatory Signaling. J Med Food. 2013 Dec 10.
  42. Kim OY, Lee SM, Do H, et al. Influence of quercetin-rich onion peel extracts on adipokine expression in the visceral adipose tissue of rats. Phytother Res. 2012 Mar;26(3):432-7.
  43. Kahn BB, Flier JS. Obesity and insulin resistance. J Clin Invest. 2000;106(4):473-81
  44. Arias N, Macarulla MT, Aguirre L, Martinez-Castano MG, Portillo MP. Quercetin can reduce insulin resistance without decreasing adipose tissue and skeletal muscle fat accumulation. Genes Nutr. 2014 Jan;9(1):361.
  45. Mahmoud MF, Hassan NA, El Bassossy HM, Fahmy A. Quercetin protects against diabetes-induced exaggerated vasoconstriction in rats: effect on low grade inflammation. PLoS One. 2013;8(5):e63784.
  46. Egert S, Bosy-Westphal A, Seiberl J, et al. Quercetin reduces systolic blood pressure and plasma oxidised low-density lipoprotein concentrations in overweight subjects with a high-cardiovascular disease risk phenotype: a double-blinded, placebo-controlled cross-over study. Br J Nutr. 2009 Oct;102(7):1065-74.
  47. Zahedi M, Ghiasvand R, Feizi A, Asgari G, Darvish L. Does Quercetin Improve Cardiovascular Risk factors and Inflammatory Biomarkers in Women with Type 2 Diabetes: A Double-blind Randomized Controlled Clinical Trial. Int J Prev Med. 2013 Jul;4(7):777-85.
  48. Dajas F. Life or death: neuroprotective and anticancer effects of quercetin. J Ethnopharmacol. 2012 Sep 28;143(2):383-96.
  49. Kim Y, Kim WJ, Cha EJ. Quercetin-induced Growth Inhibition in Human Bladder Cancer Cells Is Associated with an Increase in Ca-activated K Channels. Korean J Physiol Pharmacol. 2011 Oct;15(5):279-83.
  50. Sak K. Site-Specific Anticancer Effects of Dietary Flavonoid Quercetin. Nutr Cancer. 2013 Dec 30;66(2):177-93.
  51. Wenzel U, Herzog A, Kuntz S, Daniel H. Protein expression profiling identifies molecular targets of quercetin as a major dietary flavonoid in human colon cancer cells. Proteomics. 2004 Jul;4(7):2160-74.
  52. Cruz-Correa M, Shoskes DA, Sanchez P, et al. Combination treatment with curcumin and quercetin of adenomas in familial adenomatous polyposis. Clin Gastroenterol Hepatol. 2006 Aug;4(8):1035-8.
  53. Stabile LP, Siegfried JM. Estrogen receptor pathways in lung cancer. Curr Oncol Rep. 2004 Jul;6(4):259-67.
  54. Bulzomi P, Galluzzo P, Bolli A, Leone S, Acconcia F, Marino M. The pro‐apoptotic effect of quercetin in cancer cell lines requires ERβ‐dependent signals. J Cell Physiol. 2012; 227(5), 1891-8.
  55. Caltagirone S, Ranelletti FO, Rinelli A, et al. Interaction with type II estrogen binding sites and antiproliferative activity of tamoxifen and quercetin in human non-small-cell lung cancer. Am J Respir Cell Mol Biol. 1997 Jul;17(1):51-9.
  56. Scambia G, Ranelletti FO, Benedetti Panici P, et al. Quercetin inhibits the growth of a multidrug-resistant estrogen-receptor-negative MCF-7 human breast-cancer cell line expressing type II estrogen-binding sites. Cancer Chemother Pharmacol. 1991;28(4):255-8.
  57. Orsolic N, Goluza E, Dikic D, et al. Role of flavonoids on oxidative stress and mineral contents in the retinoic acid-induced bone loss model of rat. Eur J Nutr. 2013 Nov 23.
  58. Liang W, Luo Z, Ge S, et al. Oral administration of quercetin inhibits bone loss in rat model of diabetic osteopenia. Eur J Pharmacol. 2011 Nov 16;670(1):317-24.
  59. Derakhshanian H, Djalali M, Djazayery A, et al. Quercetin prevents experimental glucocorticoid-induced osteoporosis: a comparative study with alendronate. Can J Physiol Pharmacol. 2013 May;91(5):380-5.
  60. Satue M, Arriero Mdel M, Monjo M, Ramis JM. Quercitrin and taxifolin stimulate osteoblast differentiation in MC3T3-E1 cells and inhibit osteoclastogenesis in RAW 264.7 cells. Biochem Pharmacol. 2013 Nov 15;86(10):1476-86.
  61. Halasy-Nagy JM, Rodan GA, Reszka AA. Inhibition of bone resorption by alendronate and risedronate does not require osteoclast apoptosis. Bone. 2001 Dec;29(6):553-9.
  62. Tsuji M, Yamamoto H, Sato T, et al. Dietary quercetin inhibits bone loss without effect on the uterus in ovariectomized mice. J Bone Miner Metab. 2009;27(6):673-81.
  63. Lee JH, Kim GH. Evaluation of antioxidant and inhibitory activities for different subclasses flavonoids on enzymes for rheumatoid arthritis. J Food Sci. 2010 Sep;75(7):H212-7.
  64. Xiao P, Hao Y, Zhu X, Wu X. p53 contributes to quercetin-induced apoptosis in human rheumatoid arthritis fibroblast-like synoviocytes. Inflammation. 2013 Apr;36(2):272-8.
  65. Pap T, Muller-Ladner U, Gay RE, Gay S. Fibroblast biology. Role of synovial fibroblasts in the pathogenesis of rheumatoid arthritis. Arthritis Res. 2000;2(5):361-7.
  66. Huang J, Zhu M, Tao Y, et al. Therapeutic properties of quercetin on monosodium urate crystal-induced inflammation in rat. J Pharm Pharmacol. 2012 Aug;64(8):1119-27.
  67. Kanzaki N, Saito K, Maeda A, et al. Effect of a dietary supplement containing glucosamine hydrochloride, chondroitin sulfate and quercetin glycosides on symptomatic knee osteoarthritis: a randomized, double-blind, placebo-controlled study. J Sci Food Agric. 2012 Mar 15;92(4):862-9.
  68. Matsuno H, Nakamura H, Katayama K, et al. Effects of an oral administration of glucosamine-chondroitin-quercetin glucoside on the synovial fluid properties in patients with osteoarthritis and rheumatoid arthritis. Biosci Biotechnol Biochem. 2009 Feb;73(2):288-92.