Evidence map›Paper›PMID 26747000›Full record

ArticleJournal of the American Heart Association2016

Interferon-β Modulates Inflammatory Response in Cerebral Ischemia.

Ping-Chang Kuo, Barbara A Scofield, I-Chen Yu, Fen-Lei Chang, Doina Ganea, Jui-Hung Yen

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of the American Heart Association, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
6.4field-weighted citation impact, top 3% 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

46 citing papers in PubMed, 85 citations in OpenAlex.

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  10. Targeting inflammation and oxidative stress for protection against ischemic brain injury in rats using cupressuflavone.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2024
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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

6 authors at 3 institutions in 1 country.

Ping-Chang KuoDepartment of Microbiology and Immunology, Indiana University School of Medicine, Fort Wayne, IN (P.C.K., B.A.S., J.H.Y.).
Barbara A ScofieldDepartment of Microbiology and Immunology, Indiana University School of Medicine, Fort Wayne, IN (P.C.K., B.A.S., J.H.Y.).
I-Chen YuDepartment of Anatomy and Cell Biology, Indiana University School of Medicine, Fort Wayne, IN (I.C.Y.).
Fen-Lei ChangDepartment of Neurology, Indiana University School of Medicine, Fort Wayne, IN (F.L.C.).
Doina GaneaDepartment of Microbiology and Immunology, Temple University School of Medicine, Philadelphia, PA (D.G.).
Jui-Hung YenDepartment of Microbiology and Immunology, Indiana University School of Medicine, Fort Wayne, IN (P.C.K., B.A.S., J.H.Y.).
Indiana University School of MedicineIndiana University · USTemple University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundStroke is a leading cause of death in the world. In >80% of strokes, the initial acute phase of ischemic injury is due to the occlusion of a blood vessel resulting in severe focal hypoperfusion, excitotoxicity, and oxidative damage. Interferon-β (IFNβ), a cytokine with immunomodulatory properties, was approved by the US Food and Drug Administration for the treatment of relapsing-remitting multiple sclerosis for more than a decade. Its anti-inflammatory properties and well-characterized safety profile suggest that IFNβ has therapeutic potential for the treatment of ischemic stroke. METHODS AND

resultsWe investigated the therapeutic effect of IFNβ in the mouse model of transient middle cerebral artery occlusion/reperfusion. We found that IFNβ not only reduced infarct size in ischemic brains but also lessened neurological deficits in ischemic stroke animals. Further, multiple molecular mechanisms by which IFNβ modulates ischemic brain inflammation were identified. IFNβ reduced central nervous system infiltration of monocytes/macrophages, neutrophils, CD4(+) T cells, and γδ T cells; inhibited the production of inflammatory mediators; suppressed the expression of adhesion molecules on brain endothelial cells; and repressed microglia activation in the ischemic brain.

conclusionsOur results demonstrate that IFNβ exerts a protective effect against ischemic stroke through its anti-inflammatory properties and suggest that IFNβ is a potential therapeutic agent, targeting the reperfusion damage subsequent to the treatment with tissue plasminogen activator.

Indexed as

AnimalsAnti-Inflammatory AgentsBrainCD4-Positive T-LymphocytesCell Adhesion MoleculesCell LineChemotaxis, LeukocyteDisease Models, AnimalEndothelial CellsInfarction, Middle Cerebral ArteryInflammation MediatorsInterferon-betaMacrophagesMaleMice, Inbred C57BLMice, KnockoutAnti-Inflammatory AgentsCell Adhesion MoleculesIfnar1 protein, mouseInflammation MediatorsInterferon-betaNeuroprotective AgentsReceptor, Interferon alpha-betaCD4+ T cellsInterferon‐βischemic strokemicrogliamonocytes/macrophagesneuroinflammationreperfusionγδ T cells

Identifiers

PMID26747000
PMCPMC4859377
OpenAlexW2252484262

What OpenQuestion holds

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LicenceCC BY-NC
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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.