Evidence map›Paper›PMID 29603201›Full record

ArticleClinical and experimental immunology2018

PR-957 mediates neuroprotection by inhibiting Th17 differentiation and modulating cytokine production in a mouse model of ischaemic stroke.

Y Guo, X Chen, D Li, H Liu, Y Ding, R Han, Y Shi, X Ma

Open access · greenAbstract read
In one paragraph

Article in Clinical and experimental immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 17% 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, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
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  7. Article
  8. Article
  9. Th17 Cells and IL-17A in Ischemic Stroke.Molecular neurobiology · 2024
    Review
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  11. Article
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  13. Review
  14. Article
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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

8 authors at 2 institutions in 1 country.

Y GuoDepartment of Neurology and Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, China.
X ChenDepartment of Neurology and Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, China.
D LiDepartment of Neurology and Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, China.
H LiuDepartment of Neurology and Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, China.
Y DingDepartment of Neurology, Liaocheng People's Hospital, Shandong, Liaocheng, China.
R HanDepartment of Neurology and Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, China.
Y ShiDepartment of Neurology and Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, China.
X MaDepartment of Neurology and Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, China.ORCID 0000-0001-7032-4033
Tianjin Medical University General Hospital · CNLiaocheng People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute ischaemic stroke can induce secondary brain injury by activating an inflammatory response that contributes to clinical impairment. As a specific inhibitor of the immunoproteasome subunit low molecular weight polypeptide 7 (LMP7), PR-957 may participate in regulating pathophysiological and inflammatory responses in multiple diseases of the central nervous system (CNS). We investigated the neuroprotective properties of PR-957 in a mouse model of stroke, induced by middle cerebral artery occlusion (MCAO). After MCAO and injections of PR-957 or vehicle, we evaluated mice behaviourally using modified Neurological Severity Scores (mNSS) and sensorimotor tests, including the adhesive-removal test, a foot-fault test and an inclined plane test. Infarct volume was measured 24 and 72 h after MCAO. Infiltration by different lymphocyte subpopulations was evaluated by flow cytometry and immunofluorescent staining of brain tissue from the penumbral area. Quantitative real-time polymerase chain reaction analysis and enzyme-linked immunosorbent assay were used to measure the expression of proinflammatory cytokines: interkeukin (IL)-1α, IL-1β, IL-2, IL-4, IL-6, IL-10, IL-12, IL-17A, interferon (IFN)-γ, tumour necrosis factor (TNF)-α, granulocyte colony-stimulating factor (GCSF) and granulocyte-macrophage colony-stimulating factor (GM-CSF). Expression of phosphorylated signal transducer and activator of transcription 3 (pSTAT-3) protein levels in brain was measured by immunoblot. MCAO mice treated with PR-957 showed a significant decrease in infarct volume and had mild neurological deficits compared to vehicle-treated mice. PR-957 administration also significantly decreased IL-1β, IL-6, IL-12, IL-17A and TNF-α. PR-957 provides neuroprotection via inhibiting T lymphocyte infiltration and decreasing T helper type 17 (Th17) cell differentiation in MCAO mice, which may result from the reduced expression of pSTAT-3. The neuroprotective effect of PR-957 indicates its potential utility as anti-inflammatory therapy for ischaemic stroke.

Indexed as

Acute DiseaseAnimalsAnti-Inflammatory AgentsCell DifferentiationCytokinesDisease Models, AnimalHumansInflammation MediatorsIschemiaMaleMiceMice, Inbred C57BLNeuroprotectionNeuroprotective AgentsOligopeptidesSTAT3 Transcription FactorAnti-Inflammatory AgentsCytokinesInflammation MediatorsNeuroprotective AgentsOligopeptidesPR-957STAT3 Transcription FactorinflammationMCAORORγtSTAT-3Th17 cell

Identifiers

PMID29603201
PMCPMC6046491
OpenAlexW2795078865

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.