Interactions between quercetin and Warfarin for albumin binding: A new eye on food/drug interference

Bari, Lorenzo Di; Ripoli, Silvia; Pradhan, Sanghamitra; Salvadori, Piero

doi:10.1002/chir.20794

Cited by 27 publications

(20 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Thus, quercetin can effectively block the binding of albumin with curcumin, resulting in an increase in the fraction of unbound curcumin in the medium and thereby increasing the uptake of curcumin by WiDr cells. Our findings are also supported by those of recent in vitro studies, which showed that quercetin and warfarin compete for albumin bind- Bari et al, 2010). The possibility that the increase in the curcumin uptake was caused by quercetin-induced transporter inhibition (Anuchapreeda et al, 2002;Zhou et al, 2004;Li and Choi, 2009) can be excluded by considering the findings of studies on the effect of probenecid and cyclosporine A-multispecific active drug transport inhibitors (Shitara et al, 2005); these chemical inhibitors did not lead to any increase in the uptake of curcumin into WiDr cells.…”

Section: Resultssupporting

confidence: 90%

The Increased Cellular Uptake and Biliary Excretion of Curcumin by Quercetin: A Possible Role of Albumin Binding Interaction

Kim¹,

Lee²,

Lee³

et al. 2012

Drug Metab Dispos

View full text Add to dashboard Cite

ABSTRACT:Curcumin and quercetin are natural compounds with a wide spectrum of activities, including antioxidant and anticancer activities. In this study, the combined effect of the two compounds was investigated, with special emphasis on the pharmacokinetics of curcumin by the quercetin-induced changes in the albumin binding of curcumin. We evaluated the effect of quercetin on the binding of curcumin to albumin and on the uptake of curcumin into the cells of the human colon carcinoma cell line WiDr. In addition, we also investigated changes in the in vivo pharmacokinetics of curcumin and curcumin sulfate (the major metabolite of curcumin) coadministered with quercetin. We found that quercetin inhibited the binding of curcumin to albumin and increased the uptake of curcumin into WiDr cells, the human colon carcinoma cell. The quercetininduced increased uptake (1.6-fold) of curcumin into WiDr cells was also confirmed by an ex vivo study. The in vivo pharmacokinetics of curcumin showed obvious changes when it was coadministered with quercetin, with the significantly lower plasma concentration and greater biliary excretion of curcumin and curcumin sulfate. The present study suggests that quercetin could enhance the cellular uptake of curcumin and modulate in vivo pharmacokinetics of curcumin, and it could be related to albumin-binding interaction.

show abstract

Section: Resultssupporting

confidence: 90%

The Increased Cellular Uptake and Biliary Excretion of Curcumin by Quercetin: A Possible Role of Albumin Binding Interaction

Kim¹,

Lee²,

Lee³

et al. 2012

Drug Metab Dispos

View full text Add to dashboard Cite

show abstract

“…Based on a known significant overlap between the sets of proteins able to interact with warfarin and the flavonoid quercetin 32 , we hypothesized that quercetin may also interact with TG2 to alter its activity. Direct binding of quercetin to TG2 was demonstrated by a pull-down assay using quercetin-conjugated sepharose beads incubated with purified TG2 protein (Fig.…”

Section: Resultsmentioning

confidence: 99%

Transglutaminase Inhibitors Attenuate Vascular Calcification in a Preclinical Model

Beazley

Banyard

Lima

et al. 2013

ATVB

View full text Add to dashboard Cite

Objective In vitro, transglutaminase 2 (TG2)-mediated activation of the β-catenin signaling pathway is central in warfarin-induced calcification, warranting inquiry into the importance of this signaling axis as a target for preventive therapy of vascular calcification in vivo. Methods and Results The adverse effects of warfarin-induced elastocalcinosis in a rat model include calcification of the aortic media, loss of the cellular component in the vessel wall, and isolated systolic hypertension, associated with accumulation and activation of TG2 and activation of β-catenin signaling. These effects of warfarin can be completely reversed by intraperitoneal administration of the TG2-specific inhibitor KCC-009 or dietary supplementation with the bioflavonoid quercetin, known to inhibit β-catenin signaling. Our study also uncovers a previously uncharacterized ability of quercetin to inhibit TG2. Quercetin reversed the warfarin-induced increase in systolic pressure, underlying the functional consequence of this treatment. Molecular analysis shows that quercetin diet stabilizes the phenotype of smooth muscle and prevents its transformation into osteoblastic cells. Conclusions Inhibition of the TG2/β-catenin signaling axis appears to prevent warfarin-induced elastocalcinosis and to control isolated systolic hypertension.

show abstract

“…The definition of “significant” interaction in rxlist.com is that the combination potentially can cause dangerous DDI and should be used with cautions and close monitoring. It is reported that quercetin displaces warfarin bound to human serum albumin [26] due to competitive binding and that genistein also shares the binding sites in human serum albumin with warfarin [27]. It is reported that special precautions are necessary when taking dronabinol together with warfarin [28].…”

Section: Resultsmentioning

confidence: 99%

Predicting drug–drug interactions through drug structural similarities and interaction networks incorporating pharmacokinetics and pharmacodynamics knowledge

et al. 2017

View full text Add to dashboard Cite

Drug–drug interactions (DDIs) may lead to adverse effects and potentially result in drug withdrawal from the market. Predicting DDIs during drug development would help reduce development costs and time by rigorous evaluation of drug candidates. The primary mechanisms of DDIs are based on pharmacokinetics (PK) and pharmacodynamics (PD). This study examines the effects of 2D structural similarities of drugs on DDI prediction through interaction networks including both PD and PK knowledge. Our assumption was that a query drug (Dq) and a drug to be examined (De) likely have DDI if the drugs in the interaction network of De are structurally similar to Dq. A network of De describes the associations between the drugs and the proteins relating to PK and PD for De. These include target proteins, proteins interacting with target proteins, enzymes, and transporters for De. We constructed logistic regression models for DDI prediction using only 2D structural similarities between each Dq and the drugs in the network of De. The results indicated that our models could effectively predict DDIs. It was found that integrating structural similarity scores of the drugs relating to both PK and PD of De was crucial for model performance. In particular, the combination of the target- and enzyme-related scores provided the largest increase of the predictive power.Graphical abstract. Electronic supplementary materialThe online version of this article (doi:10.1186/s13321-017-0200-8) contains supplementary material, which is available to authorized users.

show abstract

Interactions between quercetin and Warfarin for albumin binding: A new eye on food/drug interference

Cited by 27 publications

References 17 publications

The Increased Cellular Uptake and Biliary Excretion of Curcumin by Quercetin: A Possible Role of Albumin Binding Interaction

The Increased Cellular Uptake and Biliary Excretion of Curcumin by Quercetin: A Possible Role of Albumin Binding Interaction

Transglutaminase Inhibitors Attenuate Vascular Calcification in a Preclinical Model

Predicting drug–drug interactions through drug structural similarities and interaction networks incorporating pharmacokinetics and pharmacodynamics knowledge

Contact Info

Product

Resources

About