Evidence map›Paper›PMID 25033388›Full record

ArticlePloS one2014

Edaravone protects against methylglyoxal-induced barrier damage in human brain endothelial cells.

Andrea E Tóth, Fruzsina R Walter, Alexandra Bocsik, Petra Sántha, Szilvia Veszelka, Lajos Nagy, László G Puskás, Pierre-Olivier Couraud, Fuyuko Takata, Shinya Dohgu and 2 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.3field-weighted citation impact, top 13% 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

28 citing papers in PubMed, 42 citations in OpenAlex.

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  15. The NovelInternational journal of molecular sciences · 2020
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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

12 authors at 5 institutions in 3 countries.

Andrea E TóthInstitute of Biophysics, Biological Research Centre of the Hungarian Academy of Sciences, Szeged, Hungary.
Fruzsina R WalterInstitute of Biophysics, Biological Research Centre of the Hungarian Academy of Sciences, Szeged, Hungary.
Alexandra BocsikInstitute of Biophysics, Biological Research Centre of the Hungarian Academy of Sciences, Szeged, Hungary.
Petra SánthaInstitute of Biophysics, Biological Research Centre of the Hungarian Academy of Sciences, Szeged, Hungary.
Szilvia VeszelkaInstitute of Biophysics, Biological Research Centre of the Hungarian Academy of Sciences, Szeged, Hungary.
Lajos NagyAvidin Ltd., Szeged, Hungary.
László G PuskásAvidin Ltd., Szeged, Hungary.
Pierre-Olivier CouraudInserm, U1016, Institut Cochin, Paris, France; CNRS, UMR8104, Paris, France; Université Paris Descartes, Sorbonne Paris Cité, Paris, France.
Fuyuko TakataDepartment of Pharmaceutical Care and Health Sciences, Fukuoka University, Fukuoka, Japan.
Shinya DohguDepartment of Pharmaceutical Care and Health Sciences, Fukuoka University, Fukuoka, Japan.
Yasufumi KataokaDepartment of Pharmaceutical Care and Health Sciences, Fukuoka University, Fukuoka, Japan.
Mária A DeliInstitute of Biophysics, Biological Research Centre of the Hungarian Academy of Sciences, Szeged, Hungary.
Fukuoka University · JPInstitute of Biophysics · HUHungarian Academy of Sciences · HUHUN-REN Szegedi Biológiai Kutatóközpont · HUInserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundElevated level of reactive carbonyl species, such as methylglyoxal, triggers carbonyl stress and activates a series of inflammatory responses leading to accelerated vascular damage. Edaravone is the active substance of a Japanese medicine, which aids neurological recovery following acute brain ischemia and subsequent cerebral infarction. Our aim was to test whether edaravone can exert a protective effect on the barrier properties of human brain endothelial cells (hCMEC/D3 cell line) treated with methylglyoxal. METHODOLOGY: Cell viability was monitored in real-time by impedance-based cell electronic sensing. The barrier function of the monolayer was characterized by measurement of resistance and flux of permeability markers, and visualized by immunohistochemistry for claudin-5 and β-catenin. Cell morphology was also examined by holographic phase imaging. PRINCIPAL

findingsMethylglyoxal exerted a time- and dose-dependent toxicity on cultured human brain endothelial cells: a concentration of 600 µM resulted in about 50% toxicity, significantly reduced the integrity and increased the permeability of the barrier. The cell morphology also changed dramatically: the area of cells decreased, their optical height significantly increased. Edaravone (3 mM) provided a complete protection against the toxic effect of methylglyoxal. Co-administration of edaravone restored cell viability, barrier integrity and functions of brain endothelial cells. Similar protection was obtained by the well-known antiglycating molecule, aminoguanidine, our reference compound.

conclusionThese results indicate for the first time that edaravone is protective in carbonyl stress induced barrier damage. Our data may contribute to the development of compounds to treat brain endothelial dysfunction in carbonyl stress related diseases.

Indexed as

Antipyrinebeta CateninBlood-Brain BarrierCell LineCell SurvivalClaudin-5EdaravoneElectric ImpedanceEndothelial CellsEndothelium, VascularFree Radical ScavengersGuanidinesHumansOxidative StressPermeabilityProtective AgentsAntipyrinebeta CateninClaudin-5CLDN5 protein, humanEdaravoneFree Radical ScavengersGuanidinespimagedineProtective AgentsPyruvaldehydeReactive Oxygen Species

Identifiers

PMID25033388
PMCPMC4102474
OpenAlexW2066464050

What Socratic 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 Socratic graph.