| Description: |
Quercetin is one of the most prominent dietary antioxidants, it is claimed to exert beneficial health effects, this includes protection against various diseases such as osteoporosis, certain forms of cancer, pulmonary and cardiovascular diseases but also against aging. It 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. It also attenuated the function VEGFR, androgen receptor and the expressions of NF-κB, IL Receptor, FAK, ERK,Nrf2. |
| Targets: |
NF-kB | IL Receptor | VEGFR | FAK | ERK | Androgen Receptor | Nrf2 |
| In vitro: |
| Ophthalmic Res. 2015;53(3):109-16. | | Quercetin Inhibits Vascular Endothelial Growth Factor-Induced Choroidal and Retinal Angiogenesis in vitro.[Pubmed: 25676100] | 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 AND RESULTS:
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 μM) 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. 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 μM 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. |
|
| In vivo: |
| Pharmacogn Mag. 2015 Apr-Jun;11(42):404-9. | | Quercetin induces human colon cancer cells apoptosis by inhibiting the nuclear factor-kappa B Pathway.[Pubmed: 25829782] | 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-κB) 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-κB pathway have shown potential anti-tumor activities. However, it is not fully elucidated in colon cancer.
CONCLUSIONS:
In this study, we demonstrate that quercetin induces apoptosis in human colon cancer CACO-2 and SW-620 cells through inhibiting NF-κB 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. | | Carcinogenesis. 2001 Mar;22(3):409-14. | | Quercetin inhibits the expression and function of the androgen receptor in LNCaP prostate cancer cells.[Pubmed: 11238180] | The androgen receptor (AR) is involved in the development and progression of prostate cancer. In order to find new compounds that may present novel mechanisms to attenuate the function of AR, we investigated the effect of a natural flavonoid chemical, quercetin, on androgen action in an androgen-responsive LNCaP prostate cancer cell line.
METHODS AND RESULTS:
Western blot analysis showed that AR protein expression was inhibited by quercetin in a dose-dependent manner. To demonstrate that the repression effects on AR expression can actually reduce its function, we found that quercetin inhibited the secretion of the prostate-specific, androgen-regulated tumor markers, PSA and hK2. The mRNA levels of androgen-regulated genes such as PSA, NKX3.1 as well as ornithine decarboxylase (ODC) were down-regulated by quercetin. Transient transfections further showed that quercetin inhibited AR-mediated PSA expression at the transcription level. Finally, it was demonstrated that quercetin could repress the expression of the AR gene at the transcription level.
CONCLUSIONS:
Our result suggests that quercetin can attenuate the function of AR by repressing its expression and has the potential to become a chemopreventive and/or chemotherapeutic agent for prostate cancer. |
|
Cell. 2018 Jan 11;172(1-2):249-261.e12. doi: 10.1016/j.cell.2017.12.019.IF=36.216(2019)
Cell Metab. 2020 Mar 3;31(3):534-548.e5. doi: 10.1016/j.cmet.2020.01.002.IF=22.415(2019)
Mol Cell. 2017 Nov 16;68(4):673-685.e6. doi: 10.1016/j.molcel.2017.10.022.IF=14.548(2019)
ACS Nano. 2018 Apr 24;12(4): 3385-3396. doi: 10.1021/acsnano.7b08969.IF=13.903(2019)
Nature Plants. 2016 Dec 22;3: 16206. doi: 10.1038/nplants.2016.205.IF=13.297(2019)
Sci Adv. 2018 Oct 24;4(10): eaat6994. doi: 10.1126/sciadv.aat6994.IF=12.804(2019)
