Evidence map›Paper›PMID 32963692›Full record

ArticleOxidative medicine and cellular longevity2020

A Sphingosine-1-Phosphate Receptor Modulator Attenuated Secondary Brain Injury and Improved Neurological Functions of Mice after ICH.

T Bobinger, T Bäuerle, L Seyler, S V Horsten, S Schwab, H B Huttner, A Manaenko

Open access · hybridAbstract read
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Article in Oxidative medicine and cellular longevity, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.5field-weighted citation impact, top 29% 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

8 citing papers in PubMed, 8 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

7 authors at 1 institution in 1 country.

T BobingerDepartment of Neurology of the Friedrich-Alexander-University Erlangen-Nuremberg, Germany.
T BäuerleDepartment of Radiology of the Friedrich-Alexander-University Erlangen-Nuremberg, Germany.
L SeylerDepartment of Radiology of the Friedrich-Alexander-University Erlangen-Nuremberg, Germany.
S V HorstenDepartment of Experimental Therapy, University Hospital Erlangen, and Preclinical Experimental Animal Center, Friedrich-Alexander-University Erlangen-Nuremberg, Germany.ORCID https://orcid.org/0000-0001-6409-0664
S SchwabDepartment of Neurology of the Friedrich-Alexander-University Erlangen-Nuremberg, Germany.ORCID https://orcid.org/0000-0002-8487-1238
H B HuttnerDepartment of Neurology of the Friedrich-Alexander-University Erlangen-Nuremberg, Germany.
A ManaenkoDepartment of Neurology of the Friedrich-Alexander-University Erlangen-Nuremberg, Germany.ORCID https://orcid.org/0000-0002-6153-6226
Friedrich-Alexander-Universität Erlangen-Nürnberg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundStroke activates the immune system and induces brain infiltration by immune cells, aggravating brain injury. Poststroke immunomodulation via (S1P-)receptor modulation is beneficial; however, the S1P-modulator in clinical use (FTY-720) is unspecific, and undesirable side effects have been reported. Previously, we tested effects of a novel selective S1P-receptor modulator, Siponimod, on ICH-induced brain injury in acute stage of the disease. In the current study, we investigated whether protective effects of Siponimod, evaluated in a short-term study, will protect the brain of ICH animals at long term as well.

methods134 C57BL/6N mice were divided into sham and ICH-operated groups. Collagenase model of ICH was employed. ICH animals were divided into Siponimod treated and nontreated. Dose- and time-dependent effects of Siponimod were investigated. Contraplay between development of brain injury and the number of lymphocytes infiltrating the brain was investigated by forelimb placing, T-Maze test, brain water content calculation, MRI scanning, and immunostaining.

resultsDepending on the therapeutic strategy, Siponimod attenuated the development of brain edema, decreased ICH-induced ventriculomegaly and improved neurological functions of animals after ICH. It was associated with less lymphocytes in the brain of ICH animals.

conclusionSiponimod is able to decrease the brain injury and improves neurological functions of animals after ICH.

Indexed as

Recovery of FunctionAnimalsAzetidinesBenzyl CompoundsBrain EdemaBrain InjuriesCD3 ComplexCell CountCerebral HemorrhageCognitionDisease Models, AnimalMice, Inbred C57BLSphingosine-1-Phosphate ReceptorsAzetidinesBenzyl CompoundsCD3 ComplexsiponimodSphingosine-1-Phosphate Receptors

Identifiers

PMID32963692
PMCPMC7492867
OpenAlexW3083731135

What OpenQuestion holds

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LicenceCC BY
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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.