Evidence map›Paper›PMID 29402897›Full record

ArticleScientific reports2018

Neuroprotective effects of pifithrin-α against traumatic brain injury in the striatum through suppression of neuroinflammation, oxidative stress, autophagy, and apoptosis.

Ya-Ni Huang, Ling-Yu Yang, Nigel H Greig, Yu-Chio Wang, Chien-Cheng Lai, Jia-Yi Wang

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

38 citing papers in PubMed, 63 citations in OpenAlex.

  1. Sequential release ofMaterials today. Bio · 2026
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  9. Mechanism of Progesterone in Treatment of Traumatic Brain Injury Based on Network Pharmacology and Molecular Docking Technology.Medical science monitor : international medical journal of experimental and clinical research · 2022
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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 4 institutions in 2 countries.

Ya-Ni HuangDepartment of Nursing and Department of Optometry, Hsin Sheng Junior College of Medical Care and Management, Taoyuan City, Taiwan.
Ling-Yu YangGraduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei, Taiwan.
Nigel H GreigDrug Design & Development Section, Translational Gerontology Branch, Intramural Research Program, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA.
Yu-Chio WangGraduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei, Taiwan.
Chien-Cheng LaiDivision of Orthopedics, Department of Surgery, Far Eastern Memorial Hospital, New Taipei City, Taiwan.
Jia-Yi WangGraduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei, Taiwan. jywang2010@tmu.edu.tw.
Taipei Medical University · TWFar Eastern Memorial Hospital · TWHsin Sheng College of Medical Care and Management · TWNational Institutes of Health · US

Funding

Design And Development Of Experimental Therapeutics ((Systemic & Neurodegenerative Disorders and Alzheimer's Disease)ZIAAG000311 · NIA · NATIONAL INSTITUTE ON AGING · PI GREIG, NIGEL H. · 2009 to 2025
$16.0M
6 · The paper itself

Abstract

Cortical and hippocampal neuronal damages caused by traumatic brain injury (TBI) are associated with motor and cognitive impairments; however, only little attention paid to the striatal damage. It is known that the p53 tumor-suppressor transcription factor participated in TBI-induced secondary brain damage. We investigated how the p53 inactivator pifithrin (PFT)-α affected TBI-induced striatal neuronal damage at 24 h post-injury. Sprague-Dawley rats subjected to a controlled cortical impact were used as TBI models. We observed that p53 mRNA significantly increased, whereas p53 protein expression was distributed predominantly in neurons but not in glia cells in striatum after TBI. PFT-α improved motor deficit following TBI. PFT-α suppressed TBI-induced striatal glial activation and expression of proinflammatory cytokines. PFT-α alleviated TBI-induced oxidative damage TBI induced autophagy was evidenced by increased protein expression of Beclin-1 and shift of microtubule-associated light chain (LC)3-I to LC3-II, and decreased p62. These effects were reduced by PFT-α. Post-injury PFT-α treatment reduced the number of degenerating (FJC-positive) and apoptotic neurons. Our results suggest that PFT-α may provide neuroprotective effects via p53-dependent or -independent mechanisms depending on the cell type and timing after the TBI and can possibly be developed into a novel therapy to ameliorate TBI-induced neuronal damage.

Indexed as

AnimalsApoptosisAutophagyBenzothiazolesBlotting, WesternBrain Injuries, TraumaticDisease Models, AnimalGene Expression ProfilingGene Expression RegulationInflammationNeurogliaNeuronsNeuroprotective AgentsOxidative StressRats, Sprague-DawleyTolueneBenzothiazolesNeuroprotective AgentspifithrinTolueneTumor Suppressor Protein p53

Identifiers

PMID29402897
PMCPMC5799311
OpenAlexW2791073739

What OpenQuestion 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 OpenQuestion graph.