Product Details: Quercetin

Quercetin DISCUSSION: Quercetin is the flavone aglycone (non-sugar-bound) form of the polyphenolic flavonoid rutin. It is the major bioflavonoid in the human diet. A potent phenolic antioxidant, research also supports Quercetin's ability to stabilize the membranes of neutrophils (a kind of immune cell) and thereby balance the production of histamine and inflammatory signaling molecules.
100 Vegi-Caps AOR06002
100% Vegetarian
SUPPLEMENT FACTS:
Serving Size: 1 Capsule
    %DRI
Quercetin 500mg *
*Dietary Reference Intake not established.
Other ingredients: none. Capsule: hypromellose, water.

AOR guarantees that no ingredients not listed on the label have been added to the product. Contains no citrus, wheat, gluten, corn, nuts, dairy, soy, eggs, fish or shellfish.

Suggested Use
Take one to three capsules daily, or as directed by a qualified health care practitioner.

Main Applications
As reported by literature:
• Cardiovascular system.
• Circulation.
• Anti-carcinogenic.
• Analgesic properties.
• Antioxidant.
• Hyperglycemia.
• Allergies.

Source
Seeds of Dimorphandra mollis - citrus-free.

Pregnancy / Nursing
No studies have been conducted. Best to avoid.

Cautions
None known.

*These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease.

The information and product descriptions appearing on this website are for information purposes only, and are not intended to provide medical advice to individuals. Consult with your physician if you have any health concerns, and before initiating any new diet, exercise, supplement, or other lifestyle changes. Any reproduction in whole or part and in print or electronic form without express permission is strictly forbidden. Permission to reproduce selected material may be granted by contacting AOR Inc.  

 

Copyright © 2005, Advanced Orthomolecular Research 

 


Quercetin An Antioxidant Flavonoid
Antioxidants stop oxidants (free radicals, which disrupt the integrity of other molecules by stripping their electrons) from attacking nearby molecules, such as mitochondria, membranes, and DNA. There are many classes of dietary antioxidants, and flavonoids are one of them. Flavonoids have many phenols linked to their antioxidants.

Common sources of flavonoids are vegetables, fruits, and beverages such as wine and teas. Of the many flavonoid

powerhouses, Quercetin is a major player. Quercetin is the most widely consumed flavonoid in the diet. Quercetin has been widely used by Russians and Europeans to treat a variety of ailments.

 

Mechanism of Action

Pain and Inflammation
Quercetin decreases the production of the inflammatory mediators by inhibiting key enzymes called cyclooxygenases and lipoxygenase, which form proinflammatory eicosanoids (local microhormones) such as PGE2 and PGE2 alpha. The mechanism is similar to that of aspirin and indomethacin. Mediators such as histamine, bradykinin and PGE2 all potentiate pain through sensitization of afferent pain endings (the nerves that transmit impulses to the CNS and brain). Basically, these inflammatory mediators cause the body's pain receptors to become more sensitive. Quercetin, however, prevents the formation of those inflammatory mediators.

Allergies
Quercetin counters allergic reactions by inhibiting enzymes responsible for the production of inflammatory mediators. Also, Quercetin inhibits histamine release by stabilizing basophils and mast cells. Quercetin is widely used by those who suffer from constant allergies (such as dust) and seasonal allergies (such as hay fever).

Cardiovascular Health
In a study that was released, a longitudinal investigation of risk factors for chronic diseases in elderly men revealed that high intakes of quercetin and other flavonoids predicted lower mortality rates and incidences of heart attack (myocardial infarction). Researchers in the Netherlands believe it is possible that quercetin and other flavonoids reduce risk of heart disease by lowering the formation of plaque-building substances, specifically oxidized low density lipoprotein (LDL).

Diabetic Complications
Many of the complications associated with diabetes, such as glaucoma, cataracts, and neuropathy, are caused by the sorbitol pathway, a process through which high levels of glucose are converted to sorbitol and fructose via the enzyme aldose reductase. In experimental animals, inhibitors of aldose reductase reduce the kidney and neurological symptoms shown to increase with diabetes. Quercetin is an established aldose reductase inhibitor.

The information and product descriptions appearing on this website are for information purposes only, and are not intended to provide medical advice to individuals. Consult with your physician if you have any health concerns, and before initiating any new diet, exercise, supplement, or other lifestyle changes. Any reproduction in whole or part and in print or electronic form without express permission is strictly forbidden. Permission to reproduce selected material may be granted by contacting AOR Inc.  

Copyright © 2005, Advanced Orthomolecular Research  

 


Quercetin reduces blood pressure in hypertensive subjects.
J Nutr. 2007 Nov;137(11):2405-11.
Edwards RL, Lyon T, Litwin SE, Rabovsky A, Symons JD, Jalili T.

Epidemiological studies report that quercetin, an antioxidant flavonol found in apples, berries, and onions, is associated with reduced risk of coronary heart disease and stroke. Quercetin supplementation also reduces blood pressure in hypertensive rodents. The efficacy of quercetin supplementation to lower blood pressure in hypertensive humans has never been evaluated. We tested the hypothesis that quercetin supplementation reduces blood pressure in hypertensive patients. We then determined whether the antihypertensive effect of quercetin is associated with reductions in systemic oxidant stress. Men and women with prehypertension (n = 19) and stage 1 hypertension (n = 22) were enrolled in a randomized, double-blind, placebo-controlled, crossover study to test the efficacy of 730 mg quercetin/d for 28 d vs. placebo. Blood pressure (mm Hg, systolic/diastolic) at enrollment was 137 +/- 2/86 +/- 1 in prehypertensives and 148 +/- 2/96 +/- 1 in stage 1 hypertensive subjects. Blood pressure was not altered in prehypertensive patients after quercetin supplementation. In contrast, reductions in (P < 0.01) systolic (-7 +/- 2 mm Hg), diastolic (-5 +/- 2 mm Hg), and mean arterial pressures (-5 +/- 2 mm Hg) were observed in stage 1 hypertensive patients after quercetin treatment. However, indices of oxidant stress measured in the plasma and urine were not affected by quercetin. These data are the first to our knowledge to show that quercetin supplementation reduces blood pressure in hypertensive subjects. Contrary to animal-based studies, there was no quercetin-evoked reduction in systemic markers of oxidative stress. 


Anti-inflammatory activity of quercetin and isoquercitrin in experimental murine allergic asthma.
Infl amm. res. 2007;56:402-408.
A. P. Rogerio1, A. Kanashiro, C. Fontanari1, E. V. G. da Silva1, Y. M. Lucisano-Valim, E. G. Soares3 and L. H. Faccioli1

Objective: Eosinophils and cytokines are implicated in the pathogenesis of allergic diseases. In the present study, we investigate the anti-infl ammatory effect of quercetin and isoquercitrin in a murine model of asthma.
Methods: BALB/c mice were immunized (ovalbumin/aluminum hydroxide, s. c.), followed by two intranasal ovalbumin challenges. From day 18 to day 22 after the fi rst immunization, the mice received daily gavages of isoquercitrin (15 mg/ kg) or quercetin (10 mg/kg). Dexamethasone (1 mg/kg, s. c.) was administered as a positive control. Leucocytes were analyzed in bronchoalveolar lavage fl uid (BALF), blood and pulmonary parenchyma at 24 h after the last ovalbumin challenge. Interleukin-5 (IL-5) was analyzed in BALF and lung homogenates.
Results: In animals receiving isoquercitrin or quercetin, eosinophil counts were lower in the BALF, blood and lung parenchyma. Neutrophil counts in blood and IL-5 levels in lung homogenate were lower only in isoquercitrin-treated mice. No alterations in mononuclear cell numbers were observed.
Conclusion: Quercetin and isoquercitrin are effective eosinophilic infl ammation 


Quercetin inhibits expression of inflammatory cytokines through attenuation of NF-kappaB and p38 MAPK in HMC-1 human mast cell line.
Inflamm Res. 2007 May;56(5):210-5.
Min YD, Choi CH, Bark H, Son HY, Park HH, Lee S, Park JW, Park EK, Shin HI, Kim SH.

OBJECTIVE AND DESIGN: Mast cell-mediated allergic inflammation is involved in many diseases such as asthma, sinusitis, and rheumatoid arthritis. Mast cells induce production of pro-inflammatory cytokines with immune regulatory properties. We investigated the effect of quercetin on the expression of pro-inflammatory cytokines in human mast cell line, HMC-1.
METHODS: HMC-1 cells were stimulated with phorbol 12-myristate 13-acetate (PMA) and calcium ionophore A23187 (PMACI).
RESULTS: Quercetin decreased the gene expression and production of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-6, and IL-8 in PMACI-stimulated HMC-1 cells. Quercetin attenuated PMACI-induced activation of NF-kappaB and p38 mitogen-activated protein kinase.
CONCLUSION: Our study provides evidence that quercetin may suitable for the treatment of mast cell-derived allergic inflammatory diseases.


Quercetin induces cell cycle G(1) arrest through elevating Cdk inhibitors p21 and p27 in human hepatoma cell line (HepG2).
Methods Find Exp Clin Pharmacol. 2007 Apr;29(3):179-83.
Mu C, Jia P, Yan Z, Liu X, Li X, Liu H.

Quercetin is a flavonoid ubiquitously found in nature. The therapeutic effect of quercetin on human hepatoma cell line (HepG2) was evaluated in this study. Various groups were incubated with different doses of quercetin for 12-, 24-, 48- and 72-h time duration and compared with control groups. Dose- and time-dependent inhibition in HepG2 proliferation was found with quercetin treatment. At 48 h of incubation, 61.78% of the cells were arrested at G(1) phase with 25 microM/l quercetin while 89.62% were arrested at G(1) phase with 50 microM/l quercetin. Furthermore, the results indicate that quercetin increased the content of Cdk inhibitor p21 protein, which was correlated with the elevation in p53 levels during 12 h of incubation. In addition, quercetin also increased the level of Cdk inhibitor p27 protein during 24 h of incubation. From our results it can be concluded that quercetin blocks cell cycle progression at G(1) phase and exerts its growth-inhibitory effect through the increase of Cdk inhibitors p21 and p27 and tumor suppressor p53 in HepG2. 


Quercetin, a flavonoid antioxidant, modulates endothelium-derived nitric oxide bioavailability in diabetic rat aortas.
Nitric Oxide. 2007 Jun;16(4):442-7.
Machha A, Achike FI, Mustafa AM, Mustafa MR.

The present work examined the effect of chronic oral administration of quercetin, a flavonoid antioxidant, on blood glucose, vascular function and oxidative stress in STZ-induced diabetic rats. Male Wistar-Kyoto (WKY) rats were randomized into euglycemic, untreated diabetic, vehicle (1% w/v methylcellulose)-treated diabetic, which served as control, or quercetin (10mgkg(-1) body weight)-treated diabetic groups and treated orally for 6 weeks. Quercetin treatment reduced blood glucose level in diabetic rats. Impaired relaxations to endothelium-dependent vasodilator acetylcholine (ACh) and enhanced vasoconstriction responses to alpha(1)-adrenoceptor agonist phenylephrine (PE) in diabetic rat aortic rings were restored to euglycemic levels by quercetin treatment. Pretreatment with N(omega)-nitro-l-arginine methyl ester (l-NAME, 10muM) or methylene blue (10muM) completely blocked but indomethacin (10muM) did not affect relaxations to ACh in aortic rings from vehicle- or quercetin-treated diabetic rats. PE-induced vasoconstriction with an essentially similar magnitude in vehicle- or quercetin-treated diabetic rat aortic rings pretreated with l-NAME (10muM) plus indomethacin (10muM). Quercetin treatment reduced plasma malonaldehyde (MDA) plus 4-hydroxyalkenals (4-HNE) content as well as increased superoxide dismutase activity and total antioxidant capacity in diabetic rats. From the present study, it can be concluded that quercetin administration to diabetic rats restores vascular function, probably through enhancement in the bioavailability of endothelium-derived nitric oxide coupled to reduced blood glucose level and oxidative stress. 


Quercetin inhibits TNF-induced NF-kappaB transcription factor recruitment to proinflammatory gene promoters in murine intestinal epithelial cells.
J Nutr. 2007 May;137(5):1208-15.
Ruiz PA, Braune A, Hölzlwimmer G, Quintanilla-Fend L, Haller D.

Flavonoids may play an important role for adjunct nutritional therapy of chronic intestinal inflammation. In this study, we characterized the molecular mechanisms by which quercetin and its enteric bacterial metabolites, taxifolin, alphitonin, and 3, 4-dihydroxy-phenylacetic acid, inhibit tumor necrosis factor alpha (TNF)-induced proinflammatory gene expression in the murine small intestinal epithelial cell (IEC) line Mode-K as well as in heterozygous TNFDeltaARE/WT mice, a murine model of experimental ileitis. Quercetin inhibited TNF-induced interferon-gamma-inducible protein 10 (IP-10) and macrophage inflammatory protein 2 (MIP-2) gene expression in Mode-K cells with effective inhibitory concentration of 40 and 44 micromol/L, respectively. Interestingly, taxifolin, alphitonin, and 3,4-dihydroxy-phenylacetic acid did not inhibit TNF responses in IEC, suggesting that microbial transformation of quercetin completely abolished its anti-inflammatory effect. At the molecular level, quercetin inhibited Akt phosphorylation but did not inhibit TNF-induced RelA/I-kappaB phosphorylation and IkappaB degradation or TNF-alpha-induced nuclear factor-kappaB transcriptional activity. Most important for understanding the mechanism involved, chromatin immunoprecipitation analysis revealed inhibitory effects of quercetin on phospho-RelA recruitment to the IP-10 and MIP-2 gene promoters. In addition, and consistent with the lack of cAMP response element binding protein (CBP)/p300 recruitment and phosphorylation/acetylation of histone 3 at the promoter binding site, quercetin inhibited histone acetyl transferase activity. The oral application of quercetin to heterozygous TNFDeltaARE/WT mice [10 mg/(d x kg body wt)] significantly inhibited IP-10 and MIP-2 gene expression in primary ileal epithelial cells but did not affect tissue pathology. These studies support an anti-inflammatory effect of quercetin in epithelial cells through mechanisms that inhibit cofactor recruitment at the chromatin of proinflammatory genes. 


Effect of quercetin and Albizzia saponins on rat mast cell.
Indian J Physiol Pharmacol. 1985 Jan-Mar;29(1):43-6.
Johri RK, Zutshi U, Kameshwaran L, Atal CK.

In the present work the effect of quercetin obtained from (Allium cepa). Albizzia lebbek (crude extract of seeds) and a pure saponin fraction of Albizzia has been studied on the mast cells in the mesentery and peritoneal fluid of rats subjected to anaphylaxis. The results show a mast cell membrane stabilizing effect of these test drugs.


Mucosal mast cells. III. Effect of quercetin and other flavonoids on antigen-induced histamine secretion from rat intestinal mast cells.
J Allergy Clin Immunol. 1984 Jun;73(6):819-23.
Pearce FL, Befus AD, Bienenstock J.

Quercetin, a naturally occurring flavonol structurally related to the antiallergic drug disodium cromoglycate inhibits anaphylactic histamine release from MMC isolated from the small bowel LP of the rat previously infected with the nematode Nippostrongylus brasiliensis. This contrasts with our previous observation that cromoglycate is inactive in this system. The present effect is immediate and does not decrease on preincubation with the drug. The flavonoids acacetin , apigenin , chrysin , and phloretin also demonstrate significant activity but are less potent than quercetin. Catechin, flavone, morin, and taxifolin are inactive. These results resemble those previously reported for the human basophil. In contrast, all compounds with the possible exception of taxifolin demonstrate significant activity against rat PMC. Acacetin and chrysin are the most effective inhibitors and are more active than quercetin. Rutin (the glycane of quercetin) and phlorezin (the glycane of phloretin) are inactive in both systems. These results are discussed in terms of the functional heterogeneity of mast cells from different sources and identify a group of compounds other than doxantrazole (reported previously), which inhibit histamine secretion by MMC.
The information and product descriptions appearing on this website are for information purposes only, and are not intended to provide medical advice to individuals. Consult with your physician if you have any health concerns, and before initiating any new diet, exercise, supplement, or other lifestyle changes. Any reproduction in whole or part and in print or electronic form without express permission is strictly forbidden. Permission to reproduce selected material may be granted by contacting AOR Inc.

Copyright © 2005, Advanced Orthomolecular Research

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Public FAQs

Q: What is Sorbitol and Why Is It Used In AORs Capsules?
A: Sorbitol, also known as glucitol, is a highly ubiquitous and naturally-occurring substance found in everything from the biochemistry of the human body to apples to chewing gum. The latter of course contains the synthetic version, and in the supplement industry sorbitol is used in capsules, tablets and softgels. Its most common roles are that of a plasticizer (to reduce capsule brittleness and enhance stability) and as a humectant (to reduce long-term leakage). Sorbitol is one of the most effective and widely used substances in the world for these and other similar purposes, spanning the food, pharmaceutical, and natural supplement industries. It holds GRAS (Generally Recognized As Safe) status with the FDA in the United States and in Canada is listed on the Ministry of Health's list of Acceptable Non-medicinal Ingredients with a composition allowance of 90%, one of the highest of any non-medicinal ingredients. However, as of March of 2009, the capsules of AOR products will no longer contain sorbitol as a constituent.