Evidence map›Paper›PMID 29797311›Full record

ArticleBritish journal of pharmacology2018

The isothiocyanate sulforaphane modulates platelet function and protects against cerebral thrombotic dysfunction.

Scarlett Gillespie, Paul M Holloway, Felix Becker, Francesca Rauzi, Shantel A Vital, Kirk A Taylor, Karen Y Stokes, Michael Emerson, Felicity N E Gavins

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.7field-weighted citation impact, top 33% 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

15 citing papers in PubMed, 23 citations in OpenAlex.

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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

9 authors at 3 institutions in 3 countries.

Scarlett GillespieDivision of Brain Sciences, Imperial College London, London, UK.
Paul M HollowayDivision of Brain Sciences, Imperial College London, London, UK.
Felix BeckerDepartment of General, Visceral and Transplant Surgery, University Hospital Muenster, Muenster, Germany.
Francesca RauziPlatelet Biology Group, National Heart and Lung Institute, Imperial College London, London, UK.
Shantel A VitalDepartment of Molecular and Cellular Physiology, Louisiana State University Health Sciences Center - Shreveport, Shreveport, LA, USA.
Kirk A TaylorPlatelet Biology Group, National Heart and Lung Institute, Imperial College London, London, UK.
Karen Y StokesDepartment of Molecular and Cellular Physiology, Louisiana State University Health Sciences Center - Shreveport, Shreveport, LA, USA.
Michael EmersonPlatelet Biology Group, National Heart and Lung Institute, Imperial College London, London, UK.ORCID 0000-0002-5305-7575
Felicity N E GavinsDepartment of Molecular and Cellular Physiology, Louisiana State University Health Sciences Center - Shreveport, Shreveport, LA, USA.ORCID 0000-0001-7008-5423
Imperial College London · GBLouisiana State University Health Sciences Center Shreveport · USUniversity Hospital Münster · DE

Funding

Cerebral Microvascular Dysfunction in Sickle Cell DiseaseR56HL125572 · NHLBI · LOUISIANA STATE UNIV HSC SHREVEPORT · PI GAVINS, FELICITY NICOLA EMMA · 2015 to 2015
$363k
Medical Research Council MC_PC_12015National Centre for the Replacement, Refinement and Reduction of Animals in Research NC/M000079/1NHLBI NIH HHS R56 HL125572
6 · The paper itself

Abstract

background and purposePlatelet activation provides a critical link between inflammation and thrombosis. Sulforaphane (SFN), a naturally occurring isothiocyanate, has been shown to display both anti-inflammatory and anti-thrombotic actions in the systemic microvasculature. As inflammation promotes thrombosis and vice versa, in this study we investigated whether SFN is able to reduce inflammatory potentiation of thrombotic events, suppress platelet activation and thrombus formation in the cerebral microvasculature. EXPERIMENTAL APPROACH: Thrombosis was induced in the murine brain using the light/dye-injury model, in conjunction with LPS treatment, with and without SFN treatment. In vitro and in vivo platelet assays (aggregation, flow and other functional tests) were also employed, using both human and murine platelets. KEY

resultsSFN was found to reduce LPS-mediated enhancement of thrombus formation in the cerebral microcirculation. In tail-bleed experiments, LPS treatment prolonged bleeding time, and SFN treatment was found to protect against this LPS-induced derangement of platelet function. SFN inhibited collagen-mediated platelet aggregation in vitro and in vivo and the associated adhesion and impaired calcium signalling. Furthermore, glycoprotein VI was shown to be involved in the protective effects observed with SFN treatment. CONCLUSIONS AND IMPLICATIONS: The data presented here provide evidence for the use of SFN in preventing stroke in selected high-risk patient cohorts.

Indexed as

AnimalsBlood PlateletsBrainCalcium SignalingCerebrovascular CirculationHumansIsothiocyanatesLipopolysaccharidesL-Lactate DehydrogenaseMaleMice, Inbred C57BLMicrocirculationNeuroprotective AgentsPlatelet AggregationPlatelet Membrane GlycoproteinsSulfoxidesIsothiocyanatesLipopolysaccharidesL-Lactate DehydrogenaseNeuroprotective AgentsPlatelet Membrane Glycoproteinsplatelet membrane glycoprotein VIsulforaphaneSulfoxides

Identifiers

PMID29797311
PMCPMC6057901
OpenAlexW2803428881

What OpenQuestion holds

Textmetadata
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.