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Last Updated: 8 months ago

Possible Interaction: Quercetin and Paclitaxel

supplement:

Quercetin

Research Papers that Mention the Interaction

Similar anti-apoptotic effects were observed when Quercetin was combined with other anti-neoplastic agents: Taxol , Pirarubicin and 5-Fluorouracil (5-Fu).
PloS one  •  2014  |  View Paper
After paclitaxel combination with ketoconazole or quercetin in guinea-pigs, the cumulative biliary excretion of paclitaxel and its metabolites up to 6 h was significantly decreased by 62 and 76%, respectively.
Anti-cancer drugs  •  2005  |  View Paper
Nine phenolic antioxidants ((+)-catechin, (-)-epicatechin, fisetin, gallic acid, morin, myricetin, naringenin, quercetin and resveratrol) were tested for inhibition of paclitaxel metabolism.
Naunyn-Schmiedeberg's Archives of Pharmacology  •  2003  |  View Paper
Classical chemotherapeutic agents, cisplatin (a platinum‐based drug) and paclitaxel (a taxene‐based drug), inhibited proliferation of JAR and JEG3 cells, and when combined with quercetin , the antiproliferative effects of cisplatin and paclitaxel were enhanced for both choriocarcinoma cell lines.
Journal of cellular physiology  •  2017  |  View Paper
Although quercetin induced cell death in a dose-dependent manner, 12.5–50 μM quercetin inhibited the activity of both taxol and nocodazole to induce G2/M arrest in various cell lines.
Nutrition and cancer  •  2010  |  View Paper
Quercetin also enhanced the apoptotic effect of the chemotherapeutic agent, paclitaxel , in HA22T/VGH cells.
Nutrition and cancer  •  2006  |  View Paper
This approach is aimed toward prolonging PTX retention time in the presence of QUE and bypassing P-glycoprotein drug efflux pumps.
International journal of nanomedicine  •  2017  |  View Paper
Furthermore, quercetin administration dose-dependently suppressed the increased expression levels of PKCε and TRPV1 in the spinal cords and DRGs of paclitaxel-treated rats and mice.
Moreover, quercetin administration may inhibited the translocation of PKCε from the cytoplasm to the membrane in the spinal cord and DRG of paclitaxel-treated rats.
Quercetin administration dose-dependently raised the thresholds for heat hyperalgesia and mechanical allodynia in paclitaxel-treated rats and mice.
Acta Pharmacologica Sinica  •  2016  |  View Paper
AUC, AB% and Cmax of paclitaxel after administration of the paclitaxel or prodrug pretreated with quercetin for 3 days were much higher than those administered after 20 min.
The AB% of paclitaxel was increased significantly (P < 0.05) by quercetin from 8.0 to 10.1 and 16.2%.
The AUC of paclitaxel after administration of the prodrug to rats pretreated with quercetin was significantly (P < 0.05) higher than the prodrug control.
The absolute bioavailability (AB%) of paclitaxel pretreated with quercetin was significantly higher (P < 0.01) than the control.
The areas under the plasma concentration-time curve (AUC) and the peak concentrations (Cmax) of paclitaxel pretreated with quercetin were significantly higher (P < 0.01) than the control.
The bioavailability of paclitaxel administered as a prodrug with or without pretreatment of quercetin was remarkably higher than the control.
The plasma concentrations of paclitaxel pretreated with quercetin were increased significantly (P < 0.01 for paclitaxel; P < 0.05 for prodrug) compared to the control.
The relative bioavailability of paclitaxel after administration of the prodrug to rats pretreated with quercetin was 1.25- to 2.02-fold higher than the prodrug control.
European journal of pharmaceutics and biopharmaceutics : official journal of Arbeitsgemeinschaft fur Pharmazeutische Verfahrenstechnik e.V  •  2004  |  View Paper
In a PC-3 cancer-bearing murine model, this combination treatment exerted the most beneficial therapeutic effects, and quercetin increased the cancer cell-killing effects of paclitaxel , with nearly no side effects compared with the single paclitaxel treatment group.
Results The combined treatment with quercetin and paclitaxel significantly inhibited cell proliferation, increased apoptosis, arrested the cell cycle at the G2/M phase, inhibited cell migration, dramatically induced ER stress to occur, and increased ROS generation.
OncoTargets and therapy  •  2020  |  View Paper