Evidence map›Paper›PMID 34062090›Full record

ArticlePharmaceutical biology2021

Selenium-containing protein from selenium-enriched

Xiaojie Song, Lijun Zhang, Xin Hui, Xiangfu Sun, Juntao Yang, Jinlei Wang, Hualian Wu, Xianjun Wang, Zuncheng Zheng, Fengyuan Che and 1 more

Open access · goldAbstract read
In one paragraph

Article in Pharmaceutical biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.8field-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

12 citing papers in PubMed, 25 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

11 authors at 4 institutions in 1 country.

Xiaojie SongDepartment of Neurology, Guangzhou University of Chinese Medicine, Guangzhou, China.
Lijun ZhangDepartment of Neurology, Linyi People's Hospital, Linyi, China.
Xin HuiDepartment of Neurology, Linyi People's Hospital, Linyi, China.
Xiangfu SunDepartment of Internal Medicine, Taian Traffic Hospital, Taian, China.
Juntao YangDepartment of Internal Medicine, Taian Traffic Hospital, Taian, China.
Jinlei WangDepartment of Internal Medicine, Taian Traffic Hospital, Taian, China.
Hualian WuCAS Key Laboratory of Tropical Marine Bio-resources and Ecology (LMB-CAS), Guangdong Key Laboratory of Marine Materia Medica (LMMM-GD), South China Sea Institute of Oceanology, Chinese Academy of Sciences, Guangzhou, China.
Xianjun WangDepartment of Neurology, Linyi People's Hospital, Linyi, China.
Zuncheng ZhengDepartment of Rehabilitation, Taian City Central Hospital, Taian, China Shandong.
Fengyuan CheDepartment of Neurology, Linyi People's Hospital, Linyi, China.
Guojun WangDepartment of Neurosurgery, Taian City Central Hospital, Taian, China.
Linyi People's Hospital · CNTaian City Central Hospital · CNGuangzhou University of Chinese Medicine · CNInstitute of Oceanology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

contextSelenium-containing protein from selenium-enriched

objectiveTo verify whether Se-SP can inhibit OGD-induced neural apoptosis and explore the underlying mechanism. MATERIALS AND

methodsPrimary hippocampal neurons were separated from Sprague-Dawley (SD) rats. 95% N

resultsSe-SP significantly improved neuronal viability (from 57.2% to 94.5%) and inhibited apoptosis in OGD-treated primary neurons (from 45.6% to 6.3%), followed by improved neuronal morphology and caspases activation. Se-SP co-treatment also effectively suppressed OGD-induced DNA damage by inhibiting ROS accumulation in neurons (from 225.6% to 106.3%). Additionally, mitochondrial dysfunction was also markedly improved by Se-SP co-treatment via balancing Bcl-2 family expression. Moreover, inhibition of mitochondrial permeability transition pore (MPTP) by CsA (an MPTP inhibitor) dramatically attenuated OGD-induced ROS generation (from 100% to 56.2%), oxidative damage, mitochondrial membrane potential (MPP) loss (from 7.5% to 44.3%), and eventually reversed the neuronal toxicity and apoptosis (from 57.4% to 79.6%). DISCUSSION AND

conclusionsSe-SP showed enhanced potential to inhibit OGD-induced neurotoxicity and apoptosis by inhibiting ROS-mediated oxidative damage through regulating MPTP opening, indicating that selenium-containing protein showed broad application in the chemoprevention and chemotherapy against human ischaemic brain injury.

Indexed as

AnimalsAntioxidantsApoptosisBacterial ProteinsGlucoseHippocampusMembrane Potential, MitochondrialMitochondrial Permeability Transition PoreNeuroprotective AgentsOxidative StressOxygenRatsRats, Sprague-DawleyReactive Oxygen SpeciesSeleniumSpirulinaAntioxidantsBacterial ProteinsGlucoseMitochondrial Permeability Transition PoreNeuroprotective AgentsOxygenReactive Oxygen SpeciesSeleniumapoptosisIschaemic brain injurymitochondrial dysfunctionneurons

Identifiers

PMID34062090
PMCPMC8172226
OpenAlexW3165738392

What OpenQuestion holds

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LicenceCC BY
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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.