Quercetin

1 Achyrocline sp. 2 Aesculus sp. 3 Ailanthus sp. 4 Alchemilla sp. 5 Alchornea sp. 6 Allium sp. 7 Angelica sp. 8 Anthemis sp. 9 Anthyllis sp. 10 Arctostaphylos sp. 11 Arnica sp. 12 Asclepias sp. 13 Asplenium sp. 14 Astrantia sp. 15 Baptisia sp. 16 Bupleurum sp. 17 Calendula sp. 18 Callitris sp. 19 Calluna sp. 20 Carum sp. 21 Castanea sp. 22 Casuarina sp. 23 Chaerophyllum sp. 24 Chamomilla sp. 25 Chimaphila sp. 26 Cicuta sp. 27 Croton sp. 28 Cyamopsis sp. 29 Dendranthema sp. 30 Dryas sp. 31 Echinacea sp. 32 Epilobium sp. 33 Eucalyptus sp. 34 Euphorbia sp. 35 Fallopia sp. 36 Filipendula sp. 37 Foeniculum sp. 38 Geranium sp. 39 Ginkgo sp. 40 Glycyrrhiza sp. 41 Grindelia sp. 42 Hamamelis sp. 43 Haplopappus sp. 44 Heterotheca sp. 45 Hippophae sp. 46 Hydrophyllum sp. 47 Hypericum sp. 48 Ilex sp. 49 Inula sp. 50 Juniperus sp. 51 Larix sp. 52 Larrea sp. 53 Lycium sp. 54 Malus sp. 55 Melaleuca sp. 56 Menyanthes sp. 57 Olea sp. 58 Ononis sp. 59 Paeonia sp. 60 Persicaria sp. 61 Phyllanthus sp. 62 Pimpinella sp. 63 Pinus sp. 64 Pistacia sp. 65 Platanus sp. 66 Potentilla sp. 67 Primula sp. 68 Quercus sp. 69 Rhamnus sp. 70 Rhododendron sp. 71 Rhus sp. 72 Rosa sp. 73 Sambucus sp. 74 Sanguisorba sp. 75 Senecio sp. 76 Silybum sp. 77 Sisymbrium sp. 78 Solidago sp. 79 Sorbus sp. 80 Syzygium sp. 81 Tabebuia sp. 82 Tanacetum sp. 83 Tecoma sp. 84 Terminalia sp. 85 Tilia sp. 86 Trigonella sp. 87 Tussilago sp. 88 Vaccinium sp. 89 Verbascum sp. 90 Vincetoxicum sp. 91 Viola sp. 92 Viscum sp. 93 Zanthoxylum sp.

Quercetin, a natural flavonoid, is a stimulator of recombinant SIRT1 and also a PI3K inhibitor with IC50 of 2.4±0.6 μM, 3.0±0.0 μM and 5.4±0.3 μM for PI3K γ, PI3K δ and PI3K β, respectively.

In Vitro:Quercetin is a type of plant-based chemical, or phytochemical, used as an ingredient in supplements, beverages or foods. In several studies, it may have anti-inflammatory and antioxidant properties, and it is being investigated for a wide range of potential health benefits. Quercetin is a PI3K inhibitor with IC50 of 2.4-5.4 μM. It strongly abrogates PI3K and Src kinases, mildly inhibits Akt1/2, and slightly affected PKC, p38 and ERK1/2[1]. Quercetin inhibits TNF-induced LDH% release, EC-dependent neutrophils adhesion to bovine pulmonary artery endothelial cells (BPAEC), and BPAEC DNA synthesis and proliferation[2].

In Vivo:Combination of Quercetin (75 mg/kg) and 2-Methoxyestradiol enhances inhibition of human prostate cancer LNCaP and PC-3 cells xenograft tumor growth[3].

References:
[1]. Navarro-Nú?ez L, et al. Effect of quercetin on platelet spreading on collagen and fibrinogen and on multiple platelet kinases. Fitoterapia. 2010 Mar;81(2):75-80. [2]. Yu XB, et al. Inhibitory effects of protein kinase C inhibitors on tumor necrosis factor induced bovine pulmonary artery endothelial cell injuries. Yao Xue Xue Bao. 1996;31(3):176-81. [3]. Yang F, et al. Combination of Quercetin and 2-Methoxyestradiol Enhances Inhibition of Human Prostate Cancer LNCaP and PC-3 Cells Xenograft Tumor Growth. PLoS One. 2015 May 26;10(5):e0128277.

Quercetin inhibits vascular endothelial growth factor-induced choroidal and retinal angiogenesis in vitro.[Pubmed:25676100]

Ophthalmic Res. 2015;53(3):109-16.

PURPOSE: The aim of this study was to investigate the effects of Quercetin on vascular endothelial growth factor (VEGF)-induced choroidal and retinal angiogenesis in vitro using a rhesus macaque choroid-retinal endothelial (RF/6A) cell line. METHODS: RF/6A cells were cultured in Dulbecco's modified Eagle's medium containing 10% fetal bovine serum. Then the cells were treated with different concentrations (from 0 to 100 muM) of Quercetin and 100 ng/ml VEGF. The cell proliferation was assessed using cholecystokinin octapeptide dye. The cell migration was investigated by a Transwell assay. The tube formation was measured on Matrigel. Furthermore, the impact of Quercetin's effects on VEGF-induced activation of VEGF receptor 2 (VEGFR-2) downstream signal pathways was tested by Western blot analysis. RESULTS: Quercetin inhibits RF/6A cell proliferation in a dose-dependent fashion: 22.7, 31.5 and 36.7% inhibition on treatment with 10, 50 and 100 muM Quercetin, respectively. VEGF-induced migration and tube formation of RF/6A cells were also significantly inhibited by Quercetin in a dose-dependent manner. Quercetin inhibits VEGF-induced VEGFR-2 downstream signal pathways of RF/6A. CONCLUSIONS: The results show that Quercetin inhibits VEGF-induced cell proliferation, migration and tube formation of RF/6A. We suggest that Quercetin inhibits VEGF-induced choroidal and retinal angiogenesis in vitro. Collectively, the findings in the present study suggest that Quercetin inhibits VEGF-induced choroidal and retinal angiogenesis by targeting the VEGFR-2 pathway. This suggests that Quercetin is a choroidal and retinal angiogenesis inhibitor.

Quercetin attenuates the development of 7, 12-dimethyl benz (a) anthracene (DMBA) and croton oil-induced skin cancer in mice.[Pubmed:25859269]

J Biomed Res. 2015 Apr;29(2):139-44.

To evaluate the chemopreventive potential of Quercetin in an experimental skin carcinogenesis mouse model. Skin tumor was induced by topical application of 7, 12-dimethyl Benz (a) anthracene (DMBA) and Croton oil in Swiss albino mouse. Quercetin was orally administered at a concentration of 200 mg/kg and 400 mg/kg body weight daily for 16 weeks in mouse to evaluate chemopreventive potential. Skin cancer was assessed by histopathological analysis. We found that Quercetin reduced the tumor size and the cumulative number of papillomas. The mean latent period was significantly increased as compared to carcinogen treated controls. Quercetin significantly decreased the serum levels of glutamate oxalate transaminase, glutamate pyruvate transaminase, alkaline phosphatase and bilirubin. It significantly increased the levels of glutathione, superoxide dismutase and catalase. The elevated level of lipid peroxides in the control group was significantly inhibited by Quercetin. Futhermore, DNA damage was significantly decreased in Quercetin treated mice as compared to DMBA and croton oil treated mice. The results suggest that Quercetin exerts chemopreventive effect on DMBA and croton oil induced skin cancer in mice by increasing antioxidant activities.

Protective effects of quercetin against chronic mixed reflux esophagitis in rats by inhibiting the nuclear factor-kappaB p65 and interleukin-8 signaling pathways.[Pubmed:25858763]

J Dig Dis. 2015 Jun;16(6):319-26.

OBJECTIVE: To observe the effects of Quercetin on chronic mixed reflux esophagitis (RE) in rats by inhibiting the nuclear factor-kappaB p65 (NF-kappaBp65) and interleukin-8 (IL-8) signaling pathways. METHODS: Forty-eight healthy male Sprague-Dawley rats were randomly divided into six groups, with 8 rats in each group: the normal intact group, the sham operation group, the RE control group, the RE group treated with omeprazole or 100 mg/kg and 200 mg/kg Quercetin. The animals were sacrificed after 6 weeks of different interventions. The pathological characteristics of esophageal mucosa were observed according to the diagnostic criteria and the expressions of NF-kappaBp65 and IL-8 were assessed by immunohistochemistry and real-time polymerase chain reaction. RESULTS: Compared with the RE control group, esophageal mucosal injury was improved and the expressions of NF-kappaBp65 and IL-8 were significantly decreased in the RE group treated with omeprazole or Quercetin (P < 0.05). Compared with the omeprazole group, the gross and microscopic scores of esophageal mucosal injury and the expressions of NF-kappaBp65 and IL-8 in the 100 mg/kg and 200 mg/kg Quercetin groups were not increased (P > 0.05). There was no statistically significant difference between the RE groups treated with 100 mg/kg Quercetin and 200 mg/kg Quercetin. CONCLUSION: Quercetin can prevent esophageal mucosal injury in RE rats by suppressing the NF-kappaBp65 and IL- 8 signaling pathways.

Quercetin induces human colon cancer cells apoptosis by inhibiting the nuclear factor-kappa B Pathway.[Pubmed:25829782]

Pharmacogn Mag. 2015 Apr-Jun;11(42):404-9.

Quercetin can inhibit the growth of cancer cells with the ability to act as chemopreventers. Its cancer-preventive effect has been attributed to various mechanisms, including the induction of cell-cycle arrest and/or apoptosis as well as the antioxidant functions. Nuclear factor kappa-B (NF-kappaB) is a signaling pathway that controls transcriptional activation of genes important for tight regulation of many cellular processes and is aberrantly expressed in many types of cancer. Inhibitors of NF-kappaB pathway have shown potential anti-tumor activities. However, it is not fully elucidated in colon cancer. In this study, we demonstrate that Quercetin induces apoptosis in human colon cancer CACO-2 and SW-620 cells through inhibiting NF-kappaB pathway, as well as down-regulation of B-cell lymphoma 2 and up-regulation of Bax, thus providing basis for clinical application of Quercetin in colon cancer cases.

Quercetin inhibits the migration and proliferation of astrocytes in wound healing.[Pubmed:25793633]

Neuroreport. 2015 May 6;26(7):387-93.

A previous study showed that Quercetin inhibits astrogliosis in a scratch-wound model, but did not identify the underlying mechanisms. Here, we show that Quercetin exerts no effect on apoptosis or the viability of astrocytes, but significantly inhibits their proliferation, arresting them in the G1 phase and decreasing the percentage of cells in the S and G2 phase. In addition, we found that Quercetin significantly decreased the phosphorylation of ERK1/2 and FAK, a downstream ERK signaling protein. Inhibition of this pathway with U0126, an inhibitor of MAP kinase, retarded wound closure, whereas sustained p-ERK1/2 activation, induced by vanadate, restored astrocyte migration. Our findings thus indicate that Quercetin inhibits healing in the scratch-wound model of primary astrocytes in two ways: blockade of the G1 to S phase cell cycle transition and inhibition of the ERK/FAK signaling pathway, which may contribute toward decreasing astroglial scar formation in vivo.

The flavonol quercetin activates basolateral K(+) channels in rat distal colon epithelium.[Pubmed:11877325]

Br J Pharmacol. 2002 Mar;135(5):1183-90.

1. The flavonol Quercetin has been shown to activate a Cl(-) secretion in rat colon. Unlike the secretory activity of the related isoflavone genistein, Quercetin's secretory activity does not depend on cyclic AMP; instead, it depends on Ca(2+). We investigated the possible involvement of Ca(2+) dependent basolateral K(+) channels using apically permeabilized rat distal colon epithelium mounted in Ussing chambers. 2. In intact epithelium, Quercetin induced an increase in short-circuit current (I(sc)), which was diminished by the Cl(-) channel blockers NPPB and DPC, but not by glibenclamide, DIDS or anthracene-9-carboxylic acid. The effect of the flavonol was also inhibited by several serosally applied K(+) channel blockers (Ba(2+), quinine, clotrimazole, tetrapentylammonium, 293B), whereas other K(+) channel blockers failed to influence the Quercetin-induced increase in I(sc) (tetraethylammonium, charybdotoxin). 3. The apical membrane was permeabilized by mucosal addition of nystatin and a serosally directed K(+) gradient was applied. The successful permeabilization was confirmed by experiments demonstrating the failure of bumetanide to inhibit the carbachol-induced current. 4. In apically permeabilized epithelium, Quercetin induced a K(+) current (I(K)), which was neither influenced by ouabain nor by bumetanide. Whereas DPC, NPPB, charybdotoxin and 293B failed to inhibit this I(K), quinine, Ba(2+), clotrimazole and tetrapentylammonium were effective blockers of this current. 5. We conclude from these results that at least part of the Quercetin-induced Cl(-) secretion can be explained by an activation of basolateral K(+) channels.

Quercetin as a novel activator of L-type Ca(2+) channels in rat tail artery smooth muscle cells.[Pubmed:11934824]

Br J Pharmacol. 2002 Apr;135(7):1819-27.

1. The aim of this study was to investigate the effects of Quercetin, a natural polyphenolic flavonoid, on voltage-dependent Ca(2+) channels of smooth muscle cells freshly isolated from the rat tail artery, using either the conventional or the amphotericin B-perforated whole-cell patch-clamp method. 2. Quercetin increased L-type Ca(2+) current [I(Ca(L))] in a concentration- (pEC(50)=5.09+/-0.05) and voltage-dependent manner and shifted the maximum of the current-voltage relationship by 10 mV in the hyperpolarizing direction, without, however, modifying the threshold and the equilibrium potential for Ca(2+). 3. Quercetin-induced I(Ca(L)) stimulation was reversible upon wash-out. T-type Ca(2+) current was not affected by Quercetin. Quercetin shifted the voltage dependence of the steady-state inactivation and activation curves to more negative potentials by about 5.5 and 7.5 mV respectively, in the mid-potential of the curves as well as increasing the slope of activation. Quercetin slowed both the activation and the deactivation kinetics of the I(Ca(L)). The inactivation time course was also slowed but only at voltages higher than 10 mV. Moreover Quercetin slowed the rate of recovery from inactivation. 4. These results prove Quercetin to be a naturally-occurring L-type Ca(2+) channel activator.

Induction of apoptosis by quercetin: involvement of heat shock protein.[Pubmed:8069862]

Cancer Res. 1994 Sep 15;54(18):4952-7.

Quercetin, a widely distributed bioflavonoid, inhibits the growth of tumor cells. The present study was designed to investigate the possible involvement of apoptosis and heat shock protein in the antitumor activity of Quercetin. Treatment with Quercetin of K562, Molt-4, Raji, and MCAS tumor cell lines resulted in morphological changes, including propidium iodide-stained condensed nuclei (intact or fragmented), condensation of nuclear chromatin, and nuclear fragmentation. Agarose gel electrophoresis of Quercetin-treated tumor cells demonstrated a typical ladder-like pattern of DNA fragments. In addition, the hypodiploid DNA peak of propidium iodide-stained nuclei was revealed by flow cytometry. Quercetin induced apoptosis in cells at G1 and S in a dose- and time-dependent manner. The apoptosis-inducing activity of Quercetin was enhanced by cycloheximide and actinomycin D. A nuclease inhibitor, aurintricarboxylic acid, inhibited Quercetin-induced apoptosis, whereas deprivation of intracellular calcium by EGTA had no effect. 12-O-Tetradecanoylphorbol-13-acetate and H-7 did not affect the induction of apoptosis by Quercetin. The synthesis of HSP70 was inhibited by Quercetin when determined by immunocytochemistry, Western blot analysis, and Northern blot analysis. Quercetin-treated tumor cells were not induced to show aggregation of HSP70 in the nuclei and nucleolus in response to heat shock, resulting in apoptosis. By contrast, when tumor cells were first exposed to heat shock, no apoptosis was induced by Quercetin. In addition, pretreatment of tumor cells with HSP70 antisense oligomer that specifically inhibited the synthesis of HSP70 enhanced the subsequent induction of apoptosis by Quercetin. These results suggest that Quercetin displays antitumor activity by triggering apoptosis and that HSP70 may affect Quercetin-induced apoptosis.

Tyrosine protein kinase activity in the DMBA-induced rat mammary tumor: inhibition by quercetin.[Pubmed:6091650]

Biochem Biophys Res Commun. 1984 Sep 28;123(3):1227-33.

Tyrosine protein kinase activity was measured in membranes from DMBA-induced mammary tumors, with Angiotensin II as substrate. The apparent Km for the peptide was 3.3 mM. This enzymatic activity is inhibited by Ca+2; Mn+2 can replace Mg+2 with an increase in the Km for ATP from 47 /microM to 172 microM. The enzymatic activity was not affected by cyclic AMP but was inhibited in dose dependent manner by Quercetin, a bioflavonoid which is known to inhibit proliferation of malignant cells in vitro.

The effect of quercetin on the phosphorylation activity of the Rous sarcoma virus transforming gene product in vitro and in vivo.[Pubmed:6311542]

Eur J Biochem. 1983 Oct 3;135(3):583-9.

The phosphotransferase activity of the Rous sarcoma virus src gene product, pp60src, was inhibited both in vitro and in vivo by the bioflavonoid Quercetin. The Ki for the inhibitory effect was in the range of 6-11 microM under conditions in vitro. The inhibitory effect of Quercetin was competitive towards the nucleotides ATP and GTP as substrates for pp60src and was non-competitive towards alpha-casein as the protein substrate of this kinase activity. In contrast, studies in vitro of the phosphotransferase activity of the catalytic subunit of the cAMP-dependent protein kinase showed that this flavonoid did not inhibit the phosphorylation of physiological substrates of this enzyme. In cultured cells the half-maximal inhibition of tyrosine phosphorylation of pp60src as well as the phosphorylation of the Mr = 34000 protein, a physiological substrate of pp60src, was in the range 0.06-0.08 mM.

Quercetin, a natural flavonoid, is a stimulator of recombinant SIRT1 and also a PI3K inhibitor with IC50 of 2.4±0.6 μM, 3.0±0.0 μM and 5.4±0.3 μM for PI3K γ, PI3K δ and PI3K β, respectively.

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