Evidence map›Paper›PMID 24347822›Full record

ArticleMediators of inflammation2013

Dose-dependent anti-inflammatory and neuroprotective effects of an ανβ3 integrin-binding peptide.

Shu Han, Fan Zhang, Zhiying Hu, Yayi Sun, Jing Yang, Henry Davies, David T W Yew, Marong Fang

Open access · goldAbstract read
In one paragraph

Article in Mediators of inflammation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

16 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
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  5. Review
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  8. Article
  9. The Psoriasis Therapeutic Potential of a Novel Short Laminin Peptide C16.International journal of molecular sciences · 2019
    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 3 institutions in 1 country.

Shu HanInstitute of Neuroscience, Zhejiang University School of Medicine, 866 Yuhangtang Road, Hangzhou 310058, China.
Fan ZhangInstitute of Neuroscience, Zhejiang University School of Medicine, 866 Yuhangtang Road, Hangzhou 310058, China.
Zhiying HuDepartment of Obstetrics and Gynecology, Hangzhou Red Cross Hospital, Hangzhou 310003, China.
Yayi SunInstitute of Neuroscience, Zhejiang University School of Medicine, 866 Yuhangtang Road, Hangzhou 310058, China.
Jing YangInstitute of Neuroscience, Zhejiang University School of Medicine, 866 Yuhangtang Road, Hangzhou 310058, China.
Henry DaviesZhejiang University School of Medicine, Hangzhou 310058, China.
David T W YewBrain Research Center, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong.
Marong FangInstitute of Neuroscience, Zhejiang University School of Medicine, 866 Yuhangtang Road, Hangzhou 310058, China.
Zhejiang University · CNChinese University of Hong Kong · CNHangzhou Red Cross Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Previous studies have shown that prevention of leukocyte infiltration by targeting integrins involved in transendothelial migration may suppress the clinical and pathological features of neuroinflammatory disease. This study was designed to investigate the effects of C16, an ανβ3 integrin-binding peptide, in an acute experimental allergic encephalomyelitis (EAE) rat model. Multiple histological and immunohistochemical staining, electron microscopy observation, ELISA assay, Western blot, and magnetic resonance imaging (MRI) were employed to assess the degree of inflammation, axonal loss, neuronal apoptosis, white matter demyelination, and extent of gliosis in the brain and spinal cord of differently treated EAE models. The results showed that C16 treatment could inhibit extensive leukocyte and macrophage accumulation and infiltration and reduce cytokine tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ) expression levels. A significantly lower clinical score at the peak time of disease was also demonstrated in the C16 treated group. Moreover, astrogliosis, demyelination, neuronal death, and axonal loss were all alleviated in C16 treated EAE animals, which may be attributed to the improvement of microenvironment. The data suggests that C16 peptide may act as a protective agent by attenuating inflammatory progression and thus affecting the expression of some proinflammatory cytokines during neuroinflammatory disease.

Indexed as

AnimalsAnti-Inflammatory AgentsAxonsCarrier ProteinsDose-Response Relationship, DrugEncephalomyelitis, Autoimmune, ExperimentalIntegrin alphaVbeta3LeukocytesMaleMyelin SheathNeuroprotective AgentsRatsRats, Inbred LewAnti-Inflammatory AgentsCarrier ProteinsIntegrin alphaVbeta3Neuroprotective Agents

Identifiers

PMID24347822
PMCPMC3855988
OpenAlexW2054386607

What OpenQuestion 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 OpenQuestion graph.