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| quercetin |
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| CHEBI:16243 |
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| A pentahydroxyflavone having the five hydroxy groups placed at the 3-, 3'-, 4'-, 5- and 7-positions. It is one of the most abundant flavonoids in edible vegetables, fruit and wine. |
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This entity has been manually annotated by the ChEBI Team.
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CHEBI:45280, CHEBI:8696, CHEBI:14991, CHEBI:11704, CHEBI:26472
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| ZINC000001532656 |
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Molfile
XML
SDF
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more structures >>
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call loadScript javascripts\jsmol\core\package.js call loadScript javascripts\jsmol\core\core.z.js -- required by ClazzNode call loadScript javascripts\jsmol\J\awtjs2d\WebOutputChannel.js Jmol JavaScript applet jmolApplet0_object__214103453184066__ initializing getValue debug = null getValue logLevel = null getValue allowjavascript = null AppletRegistry.checkIn(jmolApplet0_object__214103453184066__) call loadScript javascripts\jsmol\core\corestate.z.js viewerOptions: { "name":"jmolApplet0_object","applet":true,"documentBase":"https://www.ebi.ac.uk/chebi/searchId.do?chebiId=CHEBI:16243","platform":"J.awtjs2d.Platform","fullName":"jmolApplet0_object__214103453184066__","display":"jmolApplet0_canvas2d","signedApplet":"true","appletReadyCallback":"Jmol._readyCallback","statusListener":"[J.appletjs.Jmol.MyStatusListener object]","codeBase":"https://www.ebi.ac.uk/chebi/javascripts/jsmol/","syncId":"214103453184066","bgcolor":"#000" } (C) 2012 Jmol Development Jmol Version: 13.2.7 $Date: 2013-10-01 11:35:15 -0500 (Tue, 01 Oct 2013) $ java.vendor: j2s java.version: 0.0 os.name: j2s Access: ALL memory: 0.0/0.0 processors available: 1 useCommandThread: false appletId:jmolApplet0_object (signed) starting HoverWatcher_1 getValue emulate = null defaults = "Jmol" getValue boxbgcolor = null getValue bgcolor = #000 backgroundColor = "#000" getValue ANIMFRAMECallback = null getValue APPLETREADYCallback = Jmol._readyCallback APPLETREADYCallback = "Jmol._readyCallback" getValue ATOMMOVEDCallback = null getValue CLICKCallback = null getValue ECHOCallback = null getValue ERRORCallback = null getValue EVALCallback = null getValue HOVERCallback = null getValue LOADSTRUCTCallback = null getValue MEASURECallback = null getValue MESSAGECallback = null getValue MINIMIZATIONCallback = null getValue PICKCallback = null getValue RESIZECallback = null getValue SCRIPTCallback = null getValue SYNCCallback = null getValue STRUCTUREMODIFIEDCallback = null getValue doTranslate = null language=en_US getValue popupMenu = null getValue script = null Jmol applet jmolApplet0_object__214103453184066__ ready call loadScript javascripts\jsmol\core\corescript.z.js call loadScript javascripts\jsmol\J\script\FileLoadThread.js starting QueueThread0_2 script 1 started starting HoverWatcher_3 starting HoverWatcher_4 The Resolver thinks Mol QUE - Ideal conformer Mrv1927 10272113193D starting HoverWatcher_5 Time for openFile(QUE - Ideal conformer Mrv1927 10272113193D 32 34 0 0 0 0 999 V2000 0.6370 -0.0120 4.4810 C 0 0 0 0 0 0 0 0 0 0 0 0 -0.5190 0.1190 3.7370 C 0 0 0 0 0 0 0 0 0 0 0 0 -0.4510 0.0550 2.3390 C 0 0 0 0 0 0 0 0 0 0 0 0 0.7840 -0.1420 1.6990 C 0 0 0 0 0 0 0 0 0 0 0 0 1.9350 -0.2670 2.4630 C 0 0 0 0 0 0 0 0 0 0 0 0 1.8590 -0.2080 3.8450 C 0 0 0 0 0 0 0 0 0 0 0 0 -1.6580 0.1920 1.5090 C 0 0 0 0 0 0 0 0 0 0 0 0 -1.4960 0.1140 0.1010 C 0 0 0 0 0 0 0 0 0 0 0 0 -0.2520 -0.0790 -0.4190 C 0 0 0 0 0 0 0 0 0 0 0 0 -0.1000 -0.1580 -1.8840 C 0 0 0 0 0 0 0 0 0 0 0 0 -0.9560 -0.9690 -2.6340 C 0 0 0 0 0 0 0 0 0 0 0 0 -0.8130 -1.0410 -4.0030 C 0 0 0 0 0 0 0 0 0 0 0 0 0.1800 -0.3100 -4.6390 C 0 0 0 0 0 0 0 0 0 0 0 0 1.0370 0.4990 -3.8970 C 0 0 0 0 0 0 0 0 0 0 0 0 0.8960 0.5810 -2.5250 C 0 0 0 0 0 0 0 0 0 0 0 0 0.8410 -0.2020 0.3520 O 0 0 0 0 0 0 0 0 0 0 0 0 -2.7570 0.3650 2.0120 O 0 0 0 0 0 0 0 0 0 0 0 0 2.0100 1.2140 -4.5250 O 0 0 0 0 0 0 0 0 0 0 0 0 0.3180 -0.3860 -5.9890 O 0 0 0 0 0 0 0 0 0 0 0 0 -2.5740 0.2320 -0.7200 O 0 0 0 0 0 0 0 0 0 0 0 0 2.9890 -0.3360 4.5860 O 0 0 0 0 0 0 0 0 0 0 0 0 -1.7110 0.3110 4.3550 O 0 0 0 0 0 0 0 0 0 0 0 0 0.5930 0.0350 5.5590 H 0 0 0 0 0 0 0 0 0 0 0 0 2.8900 -0.4140 1.9800 H 0 0 0 0 0 0 0 0 0 0 0 0 -1.7300 -1.5390 -2.1410 H 0 0 0 0 0 0 0 0 0 0 0 0 -1.4750 -1.6680 -4.5820 H 0 0 0 0 0 0 0 0 0 0 0 0 1.5590 1.2100 -1.9490 H 0 0 0 0 0 0 0 0 0 0 0 0 1.6240 2.0710 -4.7530 H 0 0 0 0 0 0 0 0 0 0 0 0 -0.2390 0.3080 -6.3660 H 0 0 0 0 0 0 0 0 0 0 0 0 -3.3460 0.3620 -0.1530 H 0 0 0 0 0 0 0 0 0 0 0 0 3.0940 -1.2790 4.7750 H 0 0 0 0 0 0 0 0 0 0 0 0 -1.8290 1.2660 4.4460 H 0 0 0 0 0 0 0 0 0 0 0 0 1 2 2 0 0 0 0 1 6 1 0 0 0 0 1 23 1 0 0 0 0 2 3 1 0 0 0 0 2 22 1 0 0 0 0 3 4 2 0 0 0 0 3 7 1 0 0 0 0 4 5 1 0 0 0 0 4 16 1 0 0 0 0 5 6 2 0 0 0 0 5 24 1 0 0 0 0 6 21 1 0 0 0 0 7 8 1 0 0 0 0 7 17 2 0 0 0 0 8 9 2 0 0 0 0 8 20 1 0 0 0 0 9 10 1 0 0 0 0 9 16 1 0 0 0 0 10 11 2 0 0 0 0 10 15 1 0 0 0 0 11 12 1 0 0 0 0 11 25 1 0 0 0 0 12 13 2 0 0 0 0 12 26 1 0 0 0 0 13 14 1 0 0 0 0 13 19 1 0 0 0 0 14 15 2 0 0 0 0 14 18 1 0 0 0 0 15 27 1 0 0 0 0 18 28 1 0 0 0 0 19 29 1 0 0 0 0 20 30 1 0 0 0 0 21 31 1 0 0 0 0 22 32 1 0 0 0 0 M END): 17 ms reading 32 atoms ModelSet: haveSymmetry:false haveUnitcells:false haveFractionalCoord:false 1 model in this collection. Use getProperty "modelInfo" or getProperty "auxiliaryInfo" to inspect them. Default Van der Waals type for model set to Babel 32 atoms created ModelSet: not autobonding; use forceAutobond=true to force automatic bond creation Script completed Jmol script terminated
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| Quercetin is a plant flavonol from the flavonoid group of polyphenols. It is found in many fruits, vegetables, leaves, seeds, and grains; capers, red onions, and kale are common foods containing appreciable amounts of it. It has a bitter flavor and is used as an ingredient in dietary supplements, beverages, and foods. |
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Read full article at Wikipedia
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| InChI=1S/C15H10O7/c16-7-4-10(19)12-11(5-7)22-15(14(21)13(12)20)6-1-2-8(17)9(18)3-6/h1-5,16-19,21H |
| REFJWTPEDVJJIY-UHFFFAOYSA-N |
| OC1=CC(O)=C2C(OC(=C(O)C2=O)C2=CC(O)=C(O)C=C2)=C1 |
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Mimosa diplotricha
(NCBI:txid512270)
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Found in
aerial part
(BTO:0001658).
Ethanolic extract of aerial parts
See:
PubMed
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Ophioglossum pedunculosum
(NCBI:txid60874)
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Found in
whole plant
(BTO:0001461).
75% EtOH extract of dried whole plant
See:
PubMed
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Lepisorus ussuriensis
(NCBI:txid699700)
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Found in
whole plant
(BTO:0001461).
See:
PubMed
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radical scavenger
A role played by a substance that can react readily with, and thereby eliminate, radicals.
chelator
A ligand with two or more separate binding sites that can bind to a single metallic central atom, forming a chelate.
antioxidant
A substance that opposes oxidation or inhibits reactions brought about by dioxygen or peroxides.
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plant metabolite
Any eukaryotic metabolite produced during a metabolic reaction in plants, the kingdom that include flowering plants, conifers and other gymnosperms.
EC 1.10.99.2 [ribosyldihydronicotinamide dehydrogenase (quinone)] inhibitor
An EC 1.10.99.* (oxidoreductases acting on diphenols and related substances as donors, other acceptors) inhibitor that interferes with the action of ribosyldihydronicotinamide dehydrogenase (quinone), EC 1.10.99.2.
phytoestrogen
Any compound produced by a plant that happens to have estrogenic activity.
Aurora kinase inhibitor
Any protein kinase inhibitor that inhibits the action of an Aurora kinase (a group of serine/threonine kinases that are essential for cell proliferation).
antibacterial agent
A substance (or active part thereof) that kills or slows the growth of bacteria.
protein kinase inhibitor
An EC 2.7.* (P-containing group transferase) inhibitor that interferes with the action of protein kinases.
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antineoplastic agent
A substance that inhibits or prevents the proliferation of neoplasms.
geroprotector
Any compound that supports healthy aging, slows the biological aging process, or extends lifespan.
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View more via ChEBI Ontology
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Outgoing
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quercetin
(CHEBI:16243)
has role
antibacterial agent
(CHEBI:33282)
quercetin
(CHEBI:16243)
has role
antineoplastic agent
(CHEBI:35610)
quercetin
(CHEBI:16243)
has role
antioxidant
(CHEBI:22586)
quercetin
(CHEBI:16243)
has role
Aurora kinase inhibitor
(CHEBI:70770)
quercetin
(CHEBI:16243)
has role
chelator
(CHEBI:38161)
quercetin
(CHEBI:16243)
has role
EC 1.10.99.2 [ribosyldihydronicotinamide dehydrogenase (quinone)] inhibitor
(CHEBI:77020)
quercetin
(CHEBI:16243)
has role
geroprotector
(CHEBI:176497)
quercetin
(CHEBI:16243)
has role
phytoestrogen
(CHEBI:76989)
quercetin
(CHEBI:16243)
has role
plant metabolite
(CHEBI:76924)
quercetin
(CHEBI:16243)
has role
protein kinase inhibitor
(CHEBI:37699)
quercetin
(CHEBI:16243)
has role
radical scavenger
(CHEBI:48578)
quercetin
(CHEBI:16243)
is a
7-hydroxyflavonol
(CHEBI:52267)
quercetin
(CHEBI:16243)
is a
pentahydroxyflavone
(CHEBI:25883)
quercetin
(CHEBI:16243)
is conjugate acid of
quercetin-7-olate
(CHEBI:57694)
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Incoming
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3',4',5,7-tetrahydroxy-3-methoxyflavone
(CHEBI:16860)
has functional parent
quercetin
(CHEBI:16243)
3',4',5-trihydroxy-3,7-dimethoxyflavone
(CHEBI:18010)
has functional parent
quercetin
(CHEBI:16243)
3',5-dihydroxy-3,4',7-trimethoxyflavone
(CHEBI:27825)
has functional parent
quercetin
(CHEBI:16243)
3,3'-dimethylquercetin
(CHEBI:146138)
has functional parent
quercetin
(CHEBI:16243)
8,8"-methylene-bisquercetin
(CHEBI:141141)
has functional parent
quercetin
(CHEBI:16243)
azaleatin
(CHEBI:2945)
has functional parent
quercetin
(CHEBI:16243)
cudranian 2
(CHEBI:65688)
has functional parent
quercetin
(CHEBI:16243)
isorhamnetin
(CHEBI:6052)
has functional parent
quercetin
(CHEBI:16243)
multinoside A
(CHEBI:81186)
has functional parent
quercetin
(CHEBI:16243)
ombuin
(CHEBI:67493)
has functional parent
quercetin
(CHEBI:16243)
pachypodol
(CHEBI:70007)
has functional parent
quercetin
(CHEBI:16243)
pinoquercetin
(CHEBI:8224)
has functional parent
quercetin
(CHEBI:16243)
quercetagetin
(CHEBI:8695)
has functional parent
quercetin
(CHEBI:16243)
quercetin 3,4'-dimethyl ether
(CHEBI:70008)
has functional parent
quercetin
(CHEBI:16243)
quercetin 5,7,3',4'-tetramethyl ether
(CHEBI:85124)
has functional parent
quercetin
(CHEBI:16243)
quercetin 7,3ʼ,4ʼ-trimethyl ether
(CHEBI:70024)
has functional parent
quercetin
(CHEBI:16243)
quercetin O-glycoside
(CHEBI:76424)
has functional parent
quercetin
(CHEBI:16243)
quercetin sulfate
(CHEBI:26482)
has functional parent
quercetin
(CHEBI:16243)
rhamnacene
(CHEBI:133721)
has functional parent
quercetin
(CHEBI:16243)
rhamnetin
(CHEBI:74992)
has functional parent
quercetin
(CHEBI:16243)
tamarixetin
(CHEBI:67492)
has functional parent
quercetin
(CHEBI:16243)
taxifolin
(CHEBI:38747)
has functional parent
quercetin
(CHEBI:16243)
velloquercetin
(CHEBI:9941)
has functional parent
quercetin
(CHEBI:16243)
quercetin-7-olate
(CHEBI:57694)
is conjugate base of
quercetin
(CHEBI:16243)
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2-(3,4-dihydroxyphenyl)-3,5,7-trihydroxy-4H-chromen-4-one
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2-(3,4-dihydroxyphenyl)-3,5,7-trihydroxy-4H-1-benzopyran-4-one
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ChEBI
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3,3',4',5,7-pentahydroxyflavone
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ChEBI
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3,5,7,3',4'-Pentahydroxyflavone
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KEGG COMPOUND
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3,5,7,3',4'-PENTAHYDROXYFLAVONE
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PDBeChem
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Quercetin
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KEGG COMPOUND
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sophoretin
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ChEBI
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xanthaurine
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ChEBI
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117-39-5
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CAS Registry Number
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ChemIDplus
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117-39-5
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CAS Registry Number
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NIST Chemistry WebBook
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317313
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Reaxys Registry Number
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Reaxys
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579210
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Gmelin Registry Number
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Gmelin
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Miltonprabu S, Tomczyk M, Skalicka-Woźniak K, Rastrelli L, Daglia M, Nabavi SF, Alavian SM, Nabavi SM (2017)
Hepatoprotective effect of quercetin: From chemistry to medicine.
Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association 108, 365-374 [PubMed:27591927]
[show Abstract]
Liver diseases caused by viral hepatitis infections have a negative impact on global health. Approximately 30 million people in the USA and 29 million people in the European Union suffer from chronic liver disease. There are many kinds of diseases of the liver, caused by viruses, such as hepatitis A, hepatitis B and hepatitis C, or by certain drugs and poisons including excessive alcohol consumption. Many herbal medicines are used in traditional medicine for their protective and therapeutic properties against liver diseases. Among their bioactive components, flavonoids have been found to be active against liver dysfunction and damage caused by liver diseases. Extensive evidences report that quercetin (QE), a major flavonol commonly found in apple, berries, onion, citrus fruits, cruciferous vegetables, tea, pepper, tomato, whole gain, cocoa and red wine, displays a wide range of healthy properties, including anti-oxidative, anti-inflammatory, anti-apoptotic and hepatoprotective activities against various hepatic ailments. This review aims to critically analyze the available literature regarding the hepatoprotective effects of QE with special emphasis on its mechanisms of actions. To provide a complete picture of QE, its distribution, chemistry, biosynthesis and bioavailability are reported. Overall, data in literature shows that QE appears to be a promising hepatoprotective compound. | Xingyu Z, Peijie M, Dan P, Youg W, Daojun W, Xinzheng C, Xijun Z, Yangrong S (2016)
Quercetin suppresses lung cancer growth by targeting Aurora B kinase.
Cancer medicine 5, 3156-3165 [PubMed:27704720]
[show Abstract]
aurora B kinase is highly expressed in several cancer cells and promotes tumorigenesis and progression, and therefore, it is an important target for drug to treat tumors. Quercetin was identified to be an antitumor agent. Herein, we report for the first time that quercetin inhibited aurora B activities by directly binding with aurora B in vitro and in vivo. Ex vivo studies showed that quercetin inhibited aurora B activities in JB6 Cl41 cells and A549 lung cancer cells. Moreover, knockdown of aurora B in A549 cells decreased their sensitivities to quercetin. In vivo study demonstrated that injection of quercetin in A549 tumor-bearing mice effectively suppressed cancer growth. The phosphorylation of histone 3 in tumor tissues was also decreased after quercetin treatment. In short, quercetin can suppress growth of lung cancer cells as an aurora B inhibitor both in vitro and in vivo. | Hatahet T, Morille M, Hommoss A, Devoisselle JM, Müller RH, Bégu S (2016)
Quercetin topical application, from conventional dosage forms to nanodosage forms.
European journal of pharmaceutics and biopharmaceutics : official journal of Arbeitsgemeinschaft fur Pharmazeutische Verfahrenstechnik e.V 108, 41-53 [PubMed:27565033]
[show Abstract]
Skin is a multifunctional organ with activities in protection, metabolism and regulation. Skin is in a continuous exposure to oxidizing agents and inflammogens from the sun and from the contact with the environment. These agents may overload the skin auto-defense capacity. To strengthen skin defense mechanisms against oxidation and inflammation, supplementation of exogenous antioxidants is a promising strategy. Quercetin is a flavonoid with very pronounced effective antioxidant and antiinflammatory activities, and thus a candidate of first choice for such skin supplementation. Quercetin showed interesting actions in cellular and animal based models, ranging from protecting cells from UV irradiation to support skin regeneration in wound healing. However, due to its poor solubility, quercetin has limited skin penetration ability, and various formulation approaches were taken to increase its dermal penetration. In this article, the quercetin antioxidant and antiinflammatory activities in wound healing and supporting skin against aging are discussed in detail. In addition, quercetin topical formulations from conventional emulsions to novel nanoformulations in terms of skin penetration enhancement are also presented. This article gives a comprehensive review of quercetin for topical application from biological effects to pharmaceutical formulation design for the last 25 years of research. | Khan F, Niaz K, Maqbool F, Ismail Hassan F, Abdollahi M, Nagulapalli Venkata KC, Nabavi SM, Bishayee A (2016)
Molecular Targets Underlying the Anticancer Effects of Quercetin: An Update.
Nutrients 8, E529 [PubMed:27589790]
[show Abstract]
Quercetin, a medicinally important member of the flavonoid family, is one of the most prominent dietary antioxidants. It is present in a variety of foods-including fruits, vegetables, tea, wine, as well as other dietary supplements-and is responsible for various health benefits. Numerous pharmacological effects of quercetin include protection against diseases, such as osteoporosis, certain forms of malignant tumors, and pulmonary and cardiovascular disorders. Quercetin has the special ability of scavenging highly reactive species, such as hydrogen peroxide, superoxide anion, and hydroxyl radicals. These oxygen radicals are called reactive oxygen species, which can cause oxidative damage to cellular components, such as proteins, lipids, and deoxyribonucleic acid. Various oxygen radicals play important roles in pathophysiological and degenerative processes, such as aging. Subsequently, several studies have been performed to evaluate possible advantageous health effects of quercetin and to collect scientific evidence for these beneficial health claims. These studies also gather data in order to evaluate the exact mechanism(s) of action and toxicological effects of quercetin. The purpose of this review is to present and critically analyze molecular pathways underlying the anticancer effects of quercetin. Current limitations and future directions of research on this bioactive dietary polyphenol are also critically discussed. | Ma B, Zeng J, Shao L, Zhan J (2013)
Efficient bioconversion of quercetin into a novel glycoside by Streptomyces rimosus subsp. rimosus ATCC 10970.
Journal of bioscience and bioengineering 115, 24-26 [PubMed:22920589]
[show Abstract]
Incubation of quercetin with Streptomyces rimosus subsp. rimosus ATCC 10970 yielded an unusual glycosylated derivative. The structure of the product was determined to be quercetin-7-O-β-4″-deoxy-hex-4″-enopyranosiduronic acid based on the spectral data. Quercetin was completely converted into the glycoside in 72 h. | Chan ST, Yang NC, Huang CS, Liao JW, Yeh SL (2013)
Quercetin enhances the antitumor activity of trichostatin A through upregulation of p53 protein expression in vitro and in vivo.
PloS one 8, e54255 [PubMed:23342112]
[show Abstract]
This study investigated the effects of quercetin on the anti-tumor effect of trichostatin A (TSA), a novel anticancer drug, in vitro and in vivo and the possible mechanisms of these effects in human lung cancer cells. We first showed that quercetin (5 µM) significantly increased the growth arrest and apoptosis in A549 cells (expressing wild-type p53) induced by 25 ng/mL of (82.5 nM) TSA at 48 h by about 25% and 101%, respectively. However, such enhancing effects of quercetin (5 µM) were not significant in TSA-exposed H1299 cells (a p53 null mutant) or were much lower than in A549 cells. In addition, quercetin significantly increased TSA-induced p53 expression in A549 cells. Transfection of p53 siRNA into A549 cells significantly but not completely diminished the enhancing effects of quercetin on TSA-induced apoptosis. Furthermore, we demonstrated that quercetin enhanced TSA-induced apoptosis through the mitochondrial pathway. Transfection of p53 siRNA abolished such enhancing effects of quercetin. However, quercetin increased the acetylation of histones H3 and H4 induced by TSA in A549 cells, even with p53 siRNA transfection as well as in H1299 cells. In a xenograft mouse model of lung cancer, quercetin enhanced the antitumor effect of TSA. Tumors from mice treated with TSA in combination with quercetin had higher p53 and apoptosis levels than did those from control and TSA-treated mice. These data indicate that regulation of the expression of p53 by quercetin plays an important role in enhancing TSA-induced apoptosis in A549 cells. However, p53-independent mechanisms may also contribute to the enhancing effect of quercetin. | Hoek-van den Hil EF, Keijer J, Bunschoten A, Vervoort JJ, Stankova B, Bekkenkamp M, Herreman L, Venema D, Hollman PC, Tvrzicka E, Rietjens IM, van Schothorst EM (2013)
Quercetin induces hepatic lipid omega-oxidation and lowers serum lipid levels in mice.
PloS one 8, e51588 [PubMed:23359794]
[show Abstract]
Elevated circulating lipid levels are known risk factors for cardiovascular diseases (CVD). In order to examine the effects of quercetin on lipid metabolism, mice received a mild-high-fat diet without (control) or with supplementation of 0.33% (w/w) quercetin for 12 weeks. Gas chromatography and (1)H nuclear magnetic resonance were used to quantitatively measure serum lipid profiles. Whole genome microarray analysis of liver tissue was used to identify possible mechanisms underlying altered circulating lipid levels. Body weight, energy intake and hepatic lipid accumulation did not differ significantly between the quercetin and the control group. In serum of quercetin-fed mice, triglycerides (TG) were decreased with 14% (p<0.001) and total poly unsaturated fatty acids (PUFA) were increased with 13% (p<0.01). Palmitic acid, oleic acid, and linoleic acid were all decreased by 9-15% (p<0.05) in quercetin-fed mice. Both palmitic acid and oleic acid can be oxidized by omega (ω)-oxidation. Gene expression profiling showed that quercetin increased hepatic lipid metabolism, especially ω-oxidation. At the gene level, this was reflected by the up-regulation of cytochrome P450 (Cyp) 4a10, Cyp4a14, Cyp4a31 and Acyl-CoA thioesterase 3 (Acot3). Two relevant regulators, cytochrome P450 oxidoreductase (Por, rate limiting for cytochrome P450s) and the transcription factor constitutive androstane receptor (Car; official symbol Nr1i3) were also up-regulated in the quercetin-fed mice. We conclude that quercetin intake increased hepatic lipid ω-oxidation and lowered corresponding circulating lipid levels, which may contribute to potential beneficial effects on CVD. | Pietsch K, Saul N, Menzel R, Stürzenbaum SR, Steinberg CE (2009)
Quercetin mediated lifespan extension in Caenorhabditis elegans is modulated by age-1, daf-2, sek-1 and unc-43.
Biogerontology 10, 565-578 [PubMed:19043800]
[show Abstract]
The nematode Caenorhabditis elegans responds to flavonoid-rich diets with improved health and longevity. The precise mechanism(s) responsible for this remains to be identified, but is believed to be linked to the highly antioxidative properties of flavonoids. This study provides a dissection of lifespan modulation by the flavonoid quercetin. In detail, quercetin was shown not to act as a simple antimicrobial agent or exclusively via radical scavenging capacities. Likewise, lifespan extension had no effect on reproduction and body length. Furthermore, neither a caloric restriction mimetic nor a sirtuin (sir-2.1) dependence was identified as a likely mode of action. However, four genes were pinpointed to be required for the quercetin derived lifespan extension, namely age-1, daf-2, unc-43 and sek-1. The latter two have, to date, not been linked to quercetin-mediated lifespan extension. | Krcatović E, Rusak G, Bezić N, Krajacić M (2008)
Inhibition of tobacco mosaic virus infection by quercetin and vitexin.
Acta virologica 52, 119-124 [PubMed:18564899]
[show Abstract]
The flavonoids, quercetin and vitexin were proved to reduce lesion number in the local hosts Datura stramonium and Chenopodium amaranticolor infected with Tobacco mosaic virus (TMV). Both flavonoids also reduced the virus concentration in systemically infected tobacco plants. This effect was restricted to an early stage of infection and correlated with an induced synthesis of salicylic acid (SA) and kaempferol suggesting their possible defensive role in the infected plant tissue. Since the tested flavonoids did not bind to the virus particles, their antiphytoviral activity was probably not based on a direct virus inactivation. | Davis JM, Murphy EA, McClellan JL, Carmichael MD, Gangemi JD (2008)
Quercetin reduces susceptibility to influenza infection following stressful exercise.
American journal of physiology. Regulatory, integrative and comparative physiology 295, R505-9 [PubMed:18579649]
[show Abstract]
Exercise stress is associated with increased risk for upper respiratory tract infection. We have shown that exercise stress can increase susceptibility to infection. Quercetin, a flavonoid present in a wide variety of fruits and vegetables, has been reported to inhibit infectivity and replication of a broad spectrum of viruses and may offset the increase in susceptibility to infection associated with stressful exercise. This study examined the effects of quercetin feedings on susceptibility to the influenza virus A/Puerto Rico/8/34 (H1N1) following stressful exercise. Mice were randomly assigned to one of four treatment groups: exercise-placebo, exercise-quercetin, control-placebo, or control-quercetin. Exercise consisted of a run to fatigue (approximately 140 min) on a treadmill for 3 consecutive days. Quercetin (12.5 mg/kg) was administered via gavage for 7 days before viral challenge. At 30 min after the last bout of exercise or rest, mice (n=23-30) were intranasally inoculated with a standardized dose of influenza virus (0.04 hemagglutinating units). Mice were monitored daily for morbidity (time to sickness), symptom severity, and mortality (time to death) for 21 days. Exercise stress was associated with an increased susceptibility to infection [morbidity, mortality, and symptom severity on days 5-7 (P<0.05)]; quercetin offset the increase in susceptibility to infection [morbidity, mortality, and symptom severity on days 5-7 (P<0.05)] that was associated with stressful exercise. These data suggest that short-term quercetin feedings may prove to be an effective strategy to lessen the impact of stressful exercise on susceptibility to respiratory infection. | Loke WM, Proudfoot JM, Stewart S, McKinley AJ, Needs PW, Kroon PA, Hodgson JM, Croft KD (2008)
Metabolic transformation has a profound effect on anti-inflammatory activity of flavonoids such as quercetin: lack of association between antioxidant and lipoxygenase inhibitory activity.
Biochemical pharmacology 75, 1045-1053 [PubMed:18096136]
[show Abstract]
Dietary flavonoids are thought to have health benefits possibly due to antioxidant and anti-inflammatory properties. Many previous in vitro studies examining the bioactivity of flavonoids have failed to consider the effects of metabolic transformation on flavonoid activity. In this study we examined the effect of quercetin and its major metabolites on the production of pro-inflammatory eicosanoids by human leukocytes. Studies comparing free radical scavenging, antioxidant activity and eicosanoid production demonstrate that there are different structural requirements for antioxidant and anti-inflammatory activity. We also investigated the effect of metabolic transformation on flavonoid bioactivity by comparing the activity of quercetin and its major metabolites to inhibit inflammatory eicosanoid production from human leukocytes. Quercetin was a potent inhibitor of leukotriene B4 formation in leukocytes (IC50 approximately 2 microM), and its activity was dependent on specific structural features, particularly the 2,3-double bond of the C-ring. Functionalisation of the 3'-OH group with either methyl or sulfate reduced inhibitory activity up to 50% while a glucuronide substituent at the 3-OH effectively removed the LTB4 inhibitory activity. The major quercetin metabolite quercetin-3'-O-sulfate retained considerable lipoxygenase inhibitory activity (IC50 approximately 7 microM) while quercetin-3-O-glucuronide maintained antioxidant activity but had no lipoxygenase inhibitory activity at physiological concentrations. In conclusion, we have found that structural modification of quercetin due to metabolic transformation had a profound effect on bioactivity, and that the structural features required for antioxidant activity of quercetin and related flavonoids were unrelated to those required for inhibition of inflammatory eicosanoids. | Mennen LI, Sapinho D, Ito H, Galan P, Hercberg S, Scalbert A (2008)
Urinary excretion of 13 dietary flavonoids and phenolic acids in free-living healthy subjects - variability and possible use as biomarkers of polyphenol intake.
European journal of clinical nutrition 62, 519-525 [PubMed:17426744]
[show Abstract]
ObjectiveEstimation of dietary intake of polyphenols is difficult, due to limited availability of food composition data and bias inherent to dietary assessment methods. The aim of the present study was to evaluate whether we could detect polyphenols and their metabolites in a spot urine sample in a free-living human population and whether it was related to those observed in 24-h urine samples, for potential use as a biomarkers of polyphenol intake.SubjectsFour 24-h urine samples and two spot urine samples were collected from 154 participants of the SU.VI.MAX cohort (a randomized primary-prevention trial evaluating the effect of daily antioxidant supplementation on chronic diseases) in two separate studies over, respectively, a 7- and 2-day periods. Thirteen polyphenols and metabolites (chlorogenic acid (CGA), caffeic acid (CA), m-coumaric acid (mCOU), gallic acid (GA), 4-O-methylgallic acid (MeGA), quercetin (Q), isorhamnetin (MeQ), kaempferol (K), hesperetin (HESP), naringenin (NAR), phloretin (PHLOR), enterolactone (ENL) and enterodiol (END) were measured using HPLC-ESI-MS-MS.ResultsCorrelations between the urinary excretion levels were observed. The most significant were explained by metabolic filiations (CGA/CA, CA/mCOU, GA/MeGA, Q/MeQ, NAR/PHLOR, ENL/END) or co-occurrence in a same food source (NAR/HESP). Concentrations in spot samples correlated with those in 24-h urine sample (P<0.02, except for CA and for MeQ). Intra-individual variations were smaller than inter-individual variations for all polyphenols (P<0.01) except for MeGA and for PHLOR.ConclusionThese results show that these polyphenols and metabolites are useful biomarkers for polyphenol intake. | Ogunbayo OA, Harris RM, Waring RH, Kirk CJ, Michelangeli F (2008)
Inhibition of the sarcoplasmic/endoplasmic reticulum Ca2+-ATPase by flavonoids: a quantitative structure-activity relationship study.
IUBMB life 60, 853-858 [PubMed:18785622]
[show Abstract]
Flavonoids are commonly found in fruit and vegetables and have been shown to reach concentrations of several micromolars in human blood plasma. Flavonoids are also believed to have cancer chemoprotective properties. One hypothesis is that flavonoids are able to initiate apoptosis, especially in cancer cells, via a Ca(2+)-dependent mitochondrial pathway. This pathway can be activated through an exaggerated elevation of cytosolic [Ca(2+)], and sarcoplasmic/endoplasmic reticulum Ca(2+)-ATPases (SERCA) play an essential role in ameliorating such changes. In this study, we demonstrate that flavonoids (especially flavones) can inhibit the activity of Ca(2+)-ATPases isoforms SERCA1A and SERCA2B in the micromolar concentration range. Of the 25 flavonoids tested, 3,6-dihydroxyflavone (IC(50), 4.6 microM) and 3,3',4',5,7-pentahydroxyflavone (quercetin) (IC(50), 8.9 microM) were the most potent inhibitors. We show that polyhydroxylation of the flavones are important for inhibition, with hydroxylation at position 3 (for SERCA1A) and position 6 (for SERCA2B) being particularly relevant. | Boots AW, Wilms LC, Swennen EL, Kleinjans JC, Bast A, Haenen GR (2008)
In vitro and ex vivo anti-inflammatory activity of quercetin in healthy volunteers.
Nutrition (Burbank, Los Angeles County, Calif.) 24, 703-710 [PubMed:18549926]
[show Abstract]
ObjectiveQuercetin, a commonly occurring flavonoid and well known antioxidant, has been suggested to possess other beneficial activities. The present study investigated the possible anti-inflammatory effects of physiologically attainable quercetin concentrations.MethodsThe effects of quercetin were tested in vitro, i.e., added to blood in the test tube, and ex vivo and in vivo, i.e., in blood taken after 4 wk of administration of quercetin in an intervention study.ResultsQuercetin dose-dependently inhibited in vitro lipopolysaccharide-induced tumor necrosis factor-alpha production in the blood of healthy volunteers. At a concentration of 1 muM, quercetin caused a 23% reduction. The in vitro lipopolysaccharide-induced interleukin-10 production remained unaffected by quercetin. A 4-wk quercetin intervention resulted in a significant increase in plasma quercetin concentration. The supplementation also increased total plasma antioxidant status but did not affect glutathione, vitamin C, and uric acid plasma concentrations. Basal and ex vivo lipopolysaccharide-induced tumor necrosis factor-alpha levels were not altered by the intervention.ConclusionThe present study shows that quercetin increases antioxidant capacity in vivo and displays anti-inflammatory effects in vitro, but not in vivo or ex vivo, in the blood of healthy volunteers. This lack of effect is probably due to their low cytokine and high antioxidant levels at baseline, indicating that neither inflammation nor oxidative stress is present. Only in people with increased levels of inflammation and oxidative stress, e.g., patients with a disease of which the pathology is associated with these two processes, might antioxidant supplementation be fruitful. | Lodi F, Jiménez R, Menendez C, Needs PW, Duarte J, Perez-Vizcaino F (2008)
Glucuronidated metabolites of the flavonoid quercetin do not auto-oxidise, do not generate free radicals and do not decrease nitric oxide bioavailability.
Planta medica 74, 741-746 [PubMed:18484521]
[show Abstract]
Quercetin, the most abundant flavonoid in the diet, reduces blood pressure and restores endothelial dysfunction in hypertensive animals. However, quercetin (as the aglycone) is usually not present in plasma, but it is rapidly metabolised during absorption by methylation, glucuronidation and sulfation. Depending on the experimental conditions, quercetin can show anti-oxidant or pro-oxidant effects. We have analysed the pro-oxidant effects of quercetin and its methylated (3-methylquercetin or isorhamnetin), sulfated (quercetin 3'-sulfate), glucuronidated (quercetin 3-glucuronide) and methylated plus glucuronidated (isorhamnetin 3-glucuronide) metabolites. Auto-oxidation, O(2)(-) release and NO scavenging were analysed by means of absorption spectra, lucigenin chemiluminescence or superoxide dismutase inhibitable cytochrome C reduction and an amperometric electrode, respectively. The biological activity of NO was tested in rat aortic rings. Quercetin, isorhamnetin and quercetin 3'-sulfate auto-oxidized in aqueous buffer and generated superoxide radical. Quercetin but not the glucuronide scavenged NO. In contrast, the glucuronides were without effect. Quercetin, but not quercetin 3-glucuronide, inhibited the biological activity of NO. These data indicate that, in contrast to quercetin, its main circulating forms, i. e., the glucuronides, do not exert pro-oxidant effects. | Wong RW, Rabie AB (2008)
Effect of quercetin on preosteoblasts and bone defects.
The open orthopaedics journal 2, 27-32 [PubMed:19461927]
[show Abstract]
Quercetin is a flavonol, also a phytoestrogen, available commonly in onion and apple. Our laboratory investigated its effect on MC3T3-E1 cells' alkaline phosphatase activity in vitro and compared the amount of new bone produced by quercetin in collagen matrix to that produced by bone grafts and collagen matrix in vivo. Four bone defects, 5mm by 10mm were created in the parietal bone of 2 New Zealand White rabbits. In the experimental animal, 2 defects were grafted with quercetin solution mixed with collagen matrix. In the control animal, 2 defects were grafted with collagen matrix alone. Animals were killed on day 14 and the defects were dissected and prepared for histological qualitative assessment. Results showed that 10muM of quercetin increased alkaline phosphatase activity of MC3T3-E1 cells at 72 hours in vitro by 32%. In the experimental animal, there was new bone growing inside the bone defects. In conclusion, specific concentration of quercetin increased alkaline phosphatase activity of MC3T3-E1 cells in vitro and quercetin in collagen matrix has the effect of forming new bone across bone defects in vivo. | Perez-Vizcaino F, Duarte J, Andriantsitohaina R (2006)
Endothelial function and cardiovascular disease: effects of quercetin and wine polyphenols.
Free radical research 40, 1054-1065 [PubMed:17015250]
[show Abstract]
Endothelial dysfunction is an early pathophysiological feature and independent predictor of poor prognosis in most forms of cardiovascular diseases. Epidemiological studies report an inverse association between dietary flavonoid consumption and mortality from cardiovascular diseases. In the present paper, we review the effects of flavonoids, especially quercetin and wine polyphenols, on endothelial function and dysfunction and its potential protective role in hypertension, ischemic heart disease and stroke. In vitro studies show that flavonoids may exert multiple actions on the NO-guanylyl cyclase pathway, endothelium-derived hyperpolarizing factor(s) and endothelin-1 and protect endothelial cells against apoptosis. In vivo, flavonoids prevent endothelial dysfunction and reduce blood pressure, oxidative stress and end-organ damage in hypertensive animals. Moreover, some clinical studies have shown that flavonoid-rich foods can improve endothelial function in patients with hypertension and ischemic heart disease. Altogether, the available evidence indicates that quercetin and wine polyphenols might be of therapeutic benefit in cardiovascular diseases even though prospective controlled clinical studies are still lacking. | Dávalos A, Castilla P, Gómez-Cordovés C, Bartolomé B (2006)
Quercetin is bioavailable from a single ingestion of grape juice.
International journal of food sciences and nutrition 57, 391-398 [PubMed:17135030]
[show Abstract]
The in vivo bioactivity of polyphenols will depend on their bioavailability. Grape juice is an important source of dietary phenolics. This paper reports results that prove that quercetin (3,3',4',5,7-pentahydroxyflavone) is bioavailable after a single ingestion of red grape juice by healthy volunteers. Blood plasma samples were collected before and after 2 h of ingestion of 100 ml of concentrated grape juice (n = 14), and of a placebo solution (n =6). Significant differences in the variation of the total plasma quercetin content (before and after ingestion) between the grape juice ingestion group (3.1 microg/l increase, as a mean) and the placebo group (6.0 microg/l decrease, as a mean) were found. This relatively low increase in comparison with that obtained after 2 h of ingestion of onions (201 microg/l, as a mean) and with those reported in the literature for other foods/beverages was attributed to differences in the amount of quercetin ingested, in the form in which quercetin is present, and in the food matrix. | Morales AI, Vicente-Sánchez C, Jerkic M, Santiago JM, Sánchez-González PD, Pérez-Barriocanal F, López-Novoa JM (2006)
Effect of quercetin on metallothionein, nitric oxide synthases and cyclooxygenase-2 expression on experimental chronic cadmium nephrotoxicity in rats.
Toxicology and applied pharmacology 210, 128-135 [PubMed:16226777]
[show Abstract]
Inflammation can play a key role in Cd-induced dysfunctions. Quercetin is a potent oxygen free radical scavenger and a metal chelator. Our aim was to study the effect of quercetin on Cd-induced kidney damage and metallothionein expression. The study was performed in Wistar rats that were administered during 9 weeks with either cadmium (1.2 mg Cd/kg/day, s.c.), quercetin (50 mg/kg/day, i.p.) or cadmium + quercetin. Renal toxicity was evaluated by measuring blood urea nitrogen concentration and urinary excretion of enzymes marker of tubular damage. Endothelial nitric oxide synthase (eNOS), inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) renal expression were assessed by Western blot. Renal expression of metallothionein 1 and 2 (MT-1, MT-2) and eNOS mRNA was assessed by Northern blot. Our data demonstrated that Cd-induced renal toxicity was markedly reduced in rats that also received quercetin. MT-1 and MT-2 mRNA levels in kidney were substantially increased during treatment with Cd, being even higher when the animals received Cd and quercetin. Renal eNOS expression was significantly higher in rats receiving Cd and quercetin than in animals receiving Cd alone or in control rats. In the group that received Cd, COX-2 and iNOS expression was markedly higher than in control rats. In the group Cd+quercetin, no changes in COX-2 and iNOS expression were observed compared with the control group. Our results demonstrate that quercetin treatment prevents Cd-induced overexpression of iNOS and COX-2, and increases MT expression. These effects can explain the protection by quercetin of Cd-induced nephrotoxicity. |
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