Evidence map›Paper›PMID 27401964›Full record

ArticleVascular pharmacology2016

Sulforaphane induces neurovascular protection against a systemic inflammatory challenge via both Nrf2-dependent and independent pathways.

Paul M Holloway, Scarlett Gillespie, Felix Becker, Shantel A Vital, Victoria Nguyen, J Steven Alexander, Paul C Evans, Felicity N E Gavins

Open access · greenAbstract read
In one paragraph

Article in Vascular pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 10% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.

  1. Pooled it
  2. Therapeutic Effects of Sulforaphane onInternational journal of molecular sciences · 2025
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  19. Cerebrovascular and Neurological Disorders: Protective Role of NRF2.International journal of molecular sciences · 2019
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 3 countries.

Paul M HollowayDepartment of Molecular and Cellular Physiology, Louisiana State University Health Sciences Center-Shreveport, Shreveport, LA, USA.
Scarlett GillespieDivision of Brain Sciences, Imperial College London, London, United Kingdom.
Felix BeckerDepartment of Molecular and Cellular Physiology, Louisiana State University Health Sciences Center-Shreveport, Shreveport, LA, USA; Department for General and Visceral Surgery, University Hospital Muenster, Muenster, Germany.
Shantel A VitalDepartment of Molecular and Cellular Physiology, Louisiana State University Health Sciences Center-Shreveport, Shreveport, LA, USA.
Victoria NguyenDepartment of Molecular and Cellular Physiology, Louisiana State University Health Sciences Center-Shreveport, Shreveport, LA, USA.
J Steven AlexanderDepartment of Molecular and Cellular Physiology, Louisiana State University Health Sciences Center-Shreveport, Shreveport, LA, USA.
Paul C EvansDepartment of Cardiovascular Science, University of Sheffield, Sheffield, United Kingdom.
Felicity N E GavinsDepartment of Molecular and Cellular Physiology, Louisiana State University Health Sciences Center-Shreveport, Shreveport, LA, USA; Division of Brain Sciences, Imperial College London, London, United Kingdom. Electronic address: fgavin@lsuhsc.edu.
Louisiana State University Health Sciences Center Shreveport · USImperial College London · GBUniversity of Sheffield · GB

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_12015NHLBI NIH HHS R56 HL125572
6 · The paper itself

Abstract

Sepsis is often characterized by an acute brain inflammation and dysfunction, which is associated with increased morbidity and mortality worldwide. Preventing cerebral leukocyte recruitment may provide the key to halt progression of systemic inflammation to the brain. Here we investigated the influence of the anti-inflammatory and anti-oxidant compound, sulforaphane (SFN) on lipopolysaccharide (LPS)-induced cellular interactions in the brain. The inflammatory response elicited by LPS was blunted by SFN administration (5 and 50mg/kg i.p.) 24h prior to LPS treatment in WT animals, as visualized and quantified using intravital microscopy. This protective effect of SFN was lost in Nrf2-KO mice at the lower dose tested, however 50mg/kg SFN revealed a partial effect, suggesting SFN works in part independently of Nrf2 activity. In vitro, SFN reduced neutrophil recruitment to human brain endothelial cells via a down regulation of E-selectin and vascular cell adhesion molecule 1 (VCAM-1). Our data confirm a fundamental dose-dependent role of SFN in limiting cerebral inflammation. Furthermore, our data demonstrate that not only is Nrf2 in part essential in mediating these neuroprotective effects, but they occur via down-regulation of E-selectin and VCAM-1. In conclusion, SFN may provide a useful therapeutic drug to reduce cerebral inflammation in sepsis.

Indexed as

AdolescentAdultAnimalsAnti-Inflammatory AgentsAntioxidantsBrainCell LineDisease Models, AnimalDose-Response Relationship, DrugHumansInflammationIsothiocyanatesLipopolysaccharidesMaleMiceMice, Inbred C57BLAnti-Inflammatory AgentsAntioxidantsIsothiocyanatesLipopolysaccharidesNeuroprotective AgentsNF-E2-Related Factor 2sulforaphaneSulfoxidesCerebrovascularInflammationLeukocyteNrf2Sulforaphane

Identifiers

PMID27401964
PMCPMC5021608
OpenAlexW2460151105

What OpenQuestion holds

Textmetadata
LicenceTDM
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.