Evidence map›Paper›PMID 35725978›Full record

ArticleNeurochemical research2022

Selenium Alleviates Cerebral Ischemia/Reperfusion Injury by Regulating Oxidative Stress, Mitochondrial Fusion and Ferroptosis.

Yuanyuan Shi, Lijian Han, Xianxian Zhang, Lili Xie, Pinglei Pan, Fei Chen

Open access · hybridAbstract read
In one paragraph

Article in Neurochemical research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
10.6field-weighted citation impact, top 1% 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

54 citing papers in PubMed, 98 citations in OpenAlex.

  1. Review
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  10. Traumatic brain injury-related ferroptosis: current perspectives.Journal of molecular medicine (Berlin, Germany) · 2025
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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 2 institutions in 1 country.

Yuanyuan ShiDepartment of Central Laboratory, The Yancheng School of Clinical Medicine of Nanjing Medical University (Yancheng Third People's Hospital), Yancheng, 224008, Jiangsu, China.
Lijian Han *Department of Neurology, The Yancheng School of Clinical Medicine of Nanjing Medical University (Yancheng Third People's Hospital), Yancheng, 224008, Jiangsu, China.
Xianxian ZhangDepartment of Neurology, The Yancheng School of Clinical Medicine of Nanjing Medical University (Yancheng Third People's Hospital), Yancheng, 224008, Jiangsu, China.
Lili XieDepartment of Neurology, The Yancheng School of Clinical Medicine of Nanjing Medical University (Yancheng Third People's Hospital), Yancheng, 224008, Jiangsu, China.
Pinglei PanDepartment of Central Laboratory, The Yancheng School of Clinical Medicine of Nanjing Medical University (Yancheng Third People's Hospital), Yancheng, 224008, Jiangsu, China.
Fei ChenDepartment of Central Laboratory, The Yancheng School of Clinical Medicine of Nanjing Medical University (Yancheng Third People's Hospital), Yancheng, 224008, Jiangsu, China. shuibin1988@126.com.
Yancheng Third People's Hospital · CNNanjing Medical University · CN

Funding

the Foundation Plan for Outstanding People of The Sixth Peak of Jiangsu Province of China 2019-WSN-313the Medical and Scientific Development Program of Yancheng of Jiangsu Province of China YK2021009the Programs of Scientific Research Project of Jiangsu Commission of Health of China H2019088
6 · The paper itself

Abstract

To clarify the potential role of selenium (Se) on cerebral ischemia/reperfusion (I/R) injury, we utilized mouse middle cerebral artery occlusion (MCAO) followed by reperfusion as an animal model and oxygen-glucose deprivation and reoxygenation (OGD/R) to treat N2a cells as a cell model, respectively. MCAO model was established in mice and then divided into different groups with or without Se treatment. TTC staining was used to observe whether the cerebral I/R modeling was successful, and the apoptosis level was determined by TUNEL staining. The expression of GPx-4 and p22phox was assessed by western blot. In vitro experiments, the OGD/R induced oxidative stress in N2a cells was assessed by levels of GSH/GSSG, malondialdehyde, superoxide dismutase and iron content, respectively. QRT-PCR was used to detect the mRNA levels of Cox-2, Fth1, Mfn1 and mtDNA in N2a cells. JC-1 staining and flow cytometry was performed to detect the mitochondrial membrane potential. Se treatment alleviated cerebral I/R injury and improved the survival rate of mice. Additionally, Se treatment apparently attenuated oxidative stress and inhibited iron accumulation in MCAO model mice and OGD/R model of N2a cells. In terms of its mechanism, Se could up-regulate Mfn1 expression to alleviate oxidative stress and ferroptosis by promoting mitochondrial fusion in vivo and vitro. These findings suggest that Se may have great potential in alleviating cerebral I/R injury.

Indexed as

Brain IschemiaFerroptosisReperfusion InjurySeleniumAnimalsApoptosisDisease Models, AnimalInfarction, Middle Cerebral ArteryIronMiceMitochondrial DynamicsOxidative StressIronSeleniumCerebral ischemia/reperfusionFerroptosisMfn1Mitochondrial fusionOxidative stressSelenium

Identifiers

PMID35725978
PMCPMC9470641
OpenAlexW4283167125

What OpenQuestion holds

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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.