Evidence map›Paper›PMID 35242008›Full record

ArticleFrontiers in neuroscience2022

Inhibiting Sphingosine 1-Phosphate Receptor Subtype 3 Attenuates Brain Damage During Ischemia-Reperfusion Injury by Regulating nNOS/NO and Oxidative Stress.

Xuehui Fan, Hongping Chen, Chen Xu, Yingju Wang, Pengqi Yin, Meng Li, Zhanbin Tang, Fangchao Jiang, Wan Wei, Jihe Song and 2 more

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

Article in Frontiers in neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 21% 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

6 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. 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

12 authors at 2 institutions in 1 country.

Xuehui FanDepartment of Neurology, The First Affiliated Hospital of Harbin Medical University, Harbin, China.
Hongping ChenDepartment of Neurology, The First Affiliated Hospital of Harbin Medical University, Harbin, China.
Chen XuDepartment of Neurology, The First Affiliated Hospital of Harbin Medical University, Harbin, China.
Yingju WangDepartment of Neurology, The First Affiliated Hospital of Harbin Medical University, Harbin, China.
Pengqi YinDepartment of Neurology, The First Affiliated Hospital of Harbin Medical University, Harbin, China.
Meng LiDepartment of Neurology, The First Affiliated Hospital of Harbin Medical University, Harbin, China.
Zhanbin TangDepartment of Neurology, The First Affiliated Hospital of Harbin Medical University, Harbin, China.
Fangchao JiangDepartment of Neurology, The First Affiliated Hospital of Harbin Medical University, Harbin, China.
Wan WeiDepartment of Neurology, The First Affiliated Hospital of Harbin Medical University, Harbin, China.
Jihe SongDepartment of Neurology, The First Affiliated Hospital of Harbin Medical University, Harbin, China.
Guozhong LiDepartment of Neurology, The First Affiliated Hospital of Harbin Medical University, Harbin, China.
Di ZhongDepartment of Neurology, The First Affiliated Hospital of Harbin Medical University, Harbin, China.
Harbin Medical University · CNFirst Affiliated Hospital of Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIschemic stroke (IS) is a common disease endangering human life and health. Cerebral ischemia triggers a series of complex harmful events, including excitotoxicity, inflammation and cell death, as well as increased nitric oxide production through the activation of nitric oxide synthase (NOS). Oxidative stress plays a major role in cerebral ischemia and reperfusion. Sphingosine 1-phosphate receptor subtype 3 (S1PR3), a member of S1P's G protein-coupled receptors S1PR1-S1PR5, is involved in a variety of biological effects in the body, and its role in regulating oxidative stress during cerebral ischemia and reperfusion is still unclear.

methodsTransient middle cerebral artery occlusion (tMCAO) mice were selected as the brain ischemia-reperfusion (I/R) injury model. Male C57/BL6 mice were treated with or without a selective S1PR3 inhibition after tMCAO, and changes in infarct volume, Nissl staining, hematoxylin-eosin (H&E) staining and NOS protein, nitric oxide (NO), superoxide dismutase (SOD), and malondialdehyde (MDA) content after tMCAO were observed.

resultsIn the cerebral ischemia-reperfusion model, inhibition of S1PR3 improved the infarct volume and neuronal damage in mice after tMCAO. Similarly, inhibition of S1PR3 can reduce the expression of NO synthase subtype neuronal NOS (nNOS) and reduce the production of NO after cerebral ischemia. After cerebral ischemia and reperfusion, the oxidative stress response was enhanced, and after the administration of the S1PR3 inhibitor, the SOD content increased and the MDA content decreased, indicating that S1PR3 plays an important role in regulating oxidative stress response.

conclusionInhibiting S1PR3 attenuates brain damage during I/R injury by regulating nNOS/NO and oxidative stress, which provides a potential new therapeutic target and mechanism for the clinical treatment of IS.

Indexed as

CAY-10444cerebral ischemia-reperfusion injurynitric oxideoxidative stressS1PR3

Identifiers

PMID35242008
PMCPMC8886115
OpenAlexW4226464468

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Registered trials

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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.