Evidence map›Paper›PMID 30347766›Full record

ArticleInternational journal of molecular sciences2018

Pomalidomide Ameliorates H₂O₂-Induced Oxidative Stress Injury and Cell Death in Rat Primary Cortical Neuronal Cultures by Inducing Anti-Oxidative and Anti-Apoptosis Effects.

Yan-Rou Tsai, Cheng-Fu Chang, Jing-Huei Lai, John Chung-Che Wu, Yen-Hua Chen, Shuo-Jhen Kang, Barry J Hoffer, David Tweedie, Weiming Luo, Nigel H Greig and 2 more

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

20 citing papers in PubMed, 38 citations in OpenAlex.

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  19. Graphene Nanomaterials: Synthesis, Biocompatibility, and Cytotoxicity.International journal of molecular sciences · 2018
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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 6 institutions in 2 countries.

Yan-Rou TsaiPh.D. Program for Neural Regenerative Medicine, College of Medical Science and Technology, Taipei Medical University and National Health Research Institutes, Taipei 11031, Taiwan. aggytsai@hotmail.com.
Cheng-Fu ChangCenter for Neurotrauma and Neuroregeneration, Taipei Medical University, Taipei 11031, Taiwan. chang3@ms3.hinet.net.
Jing-Huei LaiCenter for Neurotrauma and Neuroregeneration, Taipei Medical University, Taipei 11031, Taiwan. m105095006@tmu.edu.tw.
John Chung-Che WuCenter for Neurotrauma and Neuroregeneration, Taipei Medical University, Taipei 11031, Taiwan. dr.jcwu@gmail.com.
Yen-Hua ChenCenter for Neurotrauma and Neuroregeneration, Taipei Medical University, Taipei 11031, Taiwan. swallows3366@gmail.com.
Shuo-Jhen KangCenter for Neurotrauma and Neuroregeneration, Taipei Medical University, Taipei 11031, Taiwan. terbiun@gmail.com.
Barry J HofferCenter for Neurotrauma and Neuroregeneration, Taipei Medical University, Taipei 11031, Taiwan. bhoffer@intra.nida.nih.gov.
David TweedieDrug Design & Development Section, Translational Gerontology Branch, Intramural Research Program, National Institute on Aging, National Institutes of Health, Baltimore, MD 20892, USA. tweedieda@grc.nia.nih.gov.
Weiming LuoDrug Design & Development Section, Translational Gerontology Branch, Intramural Research Program, National Institute on Aging, National Institutes of Health, Baltimore, MD 20892, USA. luowe@grc.nia.nih.gov.
Nigel H GreigDrug Design & Development Section, Translational Gerontology Branch, Intramural Research Program, National Institute on Aging, National Institutes of Health, Baltimore, MD 20892, USA. greign@grc.nia.nih.gov.
Yung-Hsiao ChiangPh.D. Program for Neural Regenerative Medicine, College of Medical Science and Technology, Taipei Medical University and National Health Research Institutes, Taipei 11031, Taiwan. ychiang@tmu.edu.tw.
Kai-Yun ChenPh.D. Program for Neural Regenerative Medicine, College of Medical Science and Technology, Taipei Medical University and National Health Research Institutes, Taipei 11031, Taiwan. kychen08@tmu.edu.tw.
Taipei Medical University · TWNational Health Research Institutes · TWNational Institutes of Health · USNational Institute on Aging · USTaipei City Hospital · TWUniversity School · US

Funding

Pro-inflammatory cytokine lowering anti-inflammatory drugsZIAAG000994 · NIA · NATIONAL INSTITUTE ON AGING · PI GREIG, NIGEL H. · 2016 to 2025
$16.8M
ALZHEIMERS RESEARCH PROJECT: Alzheimer's disease drug developmentZIAAG000469 · NIA · NATIONAL INSTITUTE ON AGING · PI GREIG, NIGEL H. · 2019 to 2025
$6.7M
Ministry of Science and Technology, Taiwan MOST-102-2314-B-038-025-MY3, MOST-105-2314-532-008, MOST 107-2314-B-038-042Taipei Medical University TMU102-AE1-B27, TMU105-AE1-B03
6 · The paper itself

Abstract

Due to its high oxygen demand and abundance of peroxidation-susceptible lipid cells, the brain is particularly vulnerable to oxidative stress. Induced by a redox state imbalance involving either excessive generation of reactive oxygen species (ROS) or dysfunction of the antioxidant system, oxidative stress plays a central role in a common pathophysiology that underpins neuronal cell death in acute neurological disorders epitomized by stroke and chronic ones such as Alzheimer's disease. After cerebral ischemia, for example, inflammation bears a key responsibility in the development of permanent neurological damage. ROS are involved in the mechanism of post-ischemic inflammation. The activation of several inflammatory enzymes produces ROS, which subsequently suppress mitochondrial activity, leading to further tissue damage. Pomalidomide (POM) is a clinically available immunomodulatory and anti-inflammatory agent. Using H₂O₂-treated rat primary cortical neuronal cultures, we found POM displayed neuroprotective effects against oxidative stress and cell death that associated with changes in the nuclear factor erythroid derived 2/superoxide dismutase 2/catalase signaling pathway. POM also suppressed nuclear factor kappa-light-chain-enhancer (NF-κB) levels and significantly mitigated cortical neuronal apoptosis by regulating Bax, Cytochrome c and Poly (ADP-ribose) polymerase. In summary, POM exerted neuroprotective effects via its anti-oxidative and anti-inflammatory actions against H₂O₂-induced injury. POM consequently represents a potential therapeutic agent against brain damage and related disorders and warrants further evaluation.

Indexed as

ApoptosisAnimalsAntioxidantsCells, CulturedCerebral CortexHydrogen PeroxideNeuronsNeuroprotective AgentsOxidative StressRatsRats, Sprague-DawleyThalidomideAntioxidantsHydrogen PeroxideNeuroprotective AgentspomalidomideThalidomideischemianeurodegenerationneuroprotectionoxidative stresspomalidomidestroke

Identifiers

PMID30347766
PMCPMC6213994
OpenAlexW2896075074

What Socratic 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 Socratic graph.