Evidence map›Paper›PMID 31150474›Full record

ArticlePloS one2019

Mechanism of the efflux transport of demethoxycurcumin-O-glucuronides in HeLa cells stably transfected with UDP-glucuronosyltransferase 1A1.

Beibei Zhang, Jing Yang, Zifei Qin, Shishi Li, Jinjin Xu, Zhihong Yao, Xiaojian Zhang, Frank J Gonzalez, Xinsheng Yao

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.3field-weighted citation impact, top 54% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Metabolism and disposition of corylifol A fromXenobiotica; the fate of foreign compounds in biological systems · 2020
    Article
  3. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 2 countries.

Beibei ZhangDepartment of Pharmacy, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Jing YangDepartment of Pharmacy, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Zifei QinDepartment of Pharmacy, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.ORCID 0000-0001-8989-1986
Shishi LiCollege of Pharmacy, Jinan University, Guangzhou, China.
Jinjin XuCollege of Pharmacy, Jinan University, Guangzhou, China.
Zhihong YaoCollege of Pharmacy, Jinan University, Guangzhou, China.
Xiaojian ZhangDepartment of Pharmacy, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Frank J GonzalezLaboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America.
Xinsheng YaoCollege of Pharmacy, Jinan University, Guangzhou, China.
Jinan University · CNFirst Affiliated Hospital of Zhengzhou University · CNNational Institutes of Health · US

Funding

Xenobiotic ReceptorsZIABC005708 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI GONZALEZ, FRANK J · 2009 to 2025
$16.4M
6 · The paper itself

Abstract

Demethoxycurcumin (DMC) is a safe and natural food-coloring additive, as well as an agent with several therapeutic properties. However, extensive glucuronidation in vivo has resulted in its poor bioavailability. In this study, we aimed to investigate the formation of DMC-O-glucuronides by uridine 5'-diphospho-glucuronosyltransferase 1A1 (UGT1A1) and its transport by breast cancer resistance protein (BCRP) and multidrug resistance-associated proteins (MRPs) in HeLa cells stably transfected with UGT1A1 (named HeLa1A1 cells). The chemical inhibitors Ko143 (a selective BCRP inhibitor) and MK571 (a pan-MRP inhibitor) both induced an obvious decrease in the excretion rate of DMC-O-glucuronides and a significant increase in intracellular DMC-O-glucuronide concentrations. Furthermore, BCRP knock-down resulted in a marked reduction in the level of excreted DMC-O-glucuronides (maximal 55.6%), whereas MRP1 and MRP4 silencing significantly decreased the levels of excreted DMC-O-glucuronides (a maximum of 42.9% for MRP1 and a maximum of 29.9% for MRP3), respectively. In contrast, neither the levels of excreted DMC-O-glucuronides nor the accumulation of DMC-O-glucuronides were significantly altered in the MRP4 knock-down HeLa cells. The BCRP, MRP1 and MRP3 transporters were identified as the most important contributors to the excretion of DMC-O-glucuronides. These results may significantly contribute to improving our understanding of mechanisms underlying the cellular disposition of DMC via UGT-mediated metabolism.

Indexed as

ATP-Binding Cassette, Sub-Family C ProteinsATP Binding Cassette Transporter, Subfamily G, Member 2Biological AvailabilityDiarylheptanoidsDiketopiperazinesFood Coloring AgentsGene SilencingGlucuronidesGlucuronosyltransferaseHeLa CellsHeterocyclic Compounds, 4 or More RingsHumansNeoplasm ProteinsPropionatesProtein TransportQuinolines3-(6-isobutyl-9-methoxy-1,4-dioxo-1,2,3,4,6,7,12,12a-octahydropyrazino(1',2'-1,6)pyrido(3,4-b)indol-3-yl)propionic acid tert-butyl esterABCC4 protein, humanABCG2 protein, humanATP-Binding Cassette, Sub-Family C ProteinsATP Binding Cassette Transporter, Subfamily G, Member 2demethoxycurcuminDiarylheptanoidsDiketopiperazinesFood Coloring AgentsGlucuronidesGlucuronosyltransferaseHeterocyclic Compounds, 4 or More Ringsmultidrug resistance-associated protein 1multidrug resistance-associated protein 3Neoplasm ProteinsPropionatesQuinolinesUGT1A1 Enzymeverlukast

Identifiers

PMID31150474
PMCPMC6544300
OpenAlexW2948021746

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.