Evidence map›Paper›PMID 27131989›Full record

ArticleBrain research2016

Salubrinal reduces oxidative stress, neuroinflammation and impulsive-like behavior in a rodent model of traumatic brain injury.

Aric F Logsdon, Brandon P Lucke-Wold, Linda Nguyen, Rae R Matsumoto, Ryan C Turner, Charles L Rosen, Jason D Huber

Open access · greenAbstract read
In one paragraph

Article in Brain research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
4.2field-weighted citation impact, top 6% 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

57 citing papers in PubMed, 85 citations in OpenAlex.

  1. [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026
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  5. ISR Modulators in Neurological Diseases.Current neuropharmacology · 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

7 authors at 2 institutions in 1 country.

Aric F LogsdonDepartment of Pharmaceutical Sciences, School of Pharmacy, Health Sciences Center, West Virginia University, One Medical Center Drive, Morgantown, WV, United States; Department of Neurosurgery, School of Medicine, West Virginia University, Morgantown, WV, United States; Centers for Neuroscience, School of Medicine, West Virginia University, Morgantown, WV, United States. Electronic address: alogsdo1@mix.wvu.edu.
Brandon P Lucke-WoldDepartment of Neurosurgery, School of Medicine, West Virginia University, Morgantown, WV, United States; Centers for Neuroscience, School of Medicine, West Virginia University, Morgantown, WV, United States. Electronic address: bwold@mix.wvu.edu.
Linda NguyenDepartment of Pharmaceutical Sciences, School of Pharmacy, Health Sciences Center, West Virginia University, One Medical Center Drive, Morgantown, WV, United States. Electronic address: lnguyen1@mix.wvu.edu.
Rae R MatsumotoDean's Office, College of Pharmacy, Touro University California, Vallejo, CA, United States. Electronic address: rae.matsumoto@tu.edu.
Ryan C TurnerDepartment of Neurosurgery, School of Medicine, West Virginia University, Morgantown, WV, United States; Centers for Neuroscience, School of Medicine, West Virginia University, Morgantown, WV, United States. Electronic address: rcturner@hsc.wvu.edu.
Charles L RosenDepartment of Neurosurgery, School of Medicine, West Virginia University, Morgantown, WV, United States; Centers for Neuroscience, School of Medicine, West Virginia University, Morgantown, WV, United States. Electronic address: crosen@hsc.wvu.edu.
Jason D HuberDepartment of Pharmaceutical Sciences, School of Pharmacy, Health Sciences Center, West Virginia University, One Medical Center Drive, Morgantown, WV, United States; Department of Neurosurgery, School of Medicine, West Virginia University, Morgantown, WV, United States; Centers for Neuroscience, School of Medicine, West Virginia University, Morgantown, WV, United States. Electronic address: jdhuber@hsc.wvu.edu.
West Virginia University · USTouro University California · US

Funding

West Virginia IDEA-CTRU54GM104942 · NIGMS · WEST VIRGINIA UNIVERSITY · PI Sally Lynn Hodder · 2012 to 2026
$81.0M
WVU &MU NEW FACULTY GRANTSP20RR016477 · NCRR · MARSHALL UNIVERSITY · PI RANKIN, GARY O · 2001 to 2011
$35.5M
MT INBRE RESEARCH COREP20RR016455 · NCRR · MONTANA STATE UNIVERSITY - BOZEMAN · PI HARMSEN, ALLEN G · 2001 to 2011
$34.4M
West Virginia Flow Cytometry Core FacilityP30GM103488 · NIGMS · WEST VIRGINIA UNIVERSITY · PI GIBSON, LAURA F. · 2012 to 2016
$4.8M
Biomedical-Behavioral Interface: Prevention and Developmental Sciences TrainingT32GM081740 · NIGMS · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI PRINZ, RONALD J · 2008 to 2022
$4.5M
COBRE FOR SIGNAL TRANSDUCTION AND CANCER PHASE IIIP30RR032138 · NCRR · WEST VIRGINIA UNIVERSITY · PI GIBSON, LAURA F. · 2011 to 2011
$1.1M
NCRR NIH HHS P20 RR016455NCRR NIH HHS P20 RR016477NCRR NIH HHS P30 RR032138NIGMS NIH HHS P30 GM103488NIGMS NIH HHS T32 GM081740NIGMS NIH HHS U54 GM104942
6 · The paper itself

Abstract

Traumatic brain injury (TBI) is the leading cause of trauma related morbidity in the developed world. TBI has been shown to trigger secondary injury cascades including endoplasmic reticulum (ER) stress, oxidative stress, and neuroinflammation. The link between secondary injury cascades and behavioral outcome following TBI is poorly understood warranting further investigation. Using our validated rodent blast TBI model, we examined the interaction of secondary injury cascades following single injury and how these interactions may contribute to impulsive-like behavior after a clinically relevant repetitive TBI paradigm. We targeted these secondary pathways acutely following single injury with the cellular stress modulator, salubrinal (SAL). We examined the neuroprotective effects of SAL administration on significantly reducing ER stress: janus-N-terminal kinase (JNK) phosphorylation and C/EBP homology protein (CHOP), oxidative stress: superoxide and carbonyls, and neuroinflammation: nuclear factor kappa beta (NFκB) activity, inducible nitric oxide synthase (iNOS) protein expression, and pro-inflammatory cytokines at 24h post-TBI. We then used the more clinically relevant repeat injury paradigm and observed elevated NFκB and iNOS activity. These injury cascades were associated with impulsive-like behavior measured on the elevated plus maze. SAL administration attenuated secondary iNOS activity at 72h following repetitive TBI, and most importantly prevented impulsive-like behavior. Overall, these results suggest a link between secondary injury cascades and impulsive-like behavior that can be modulated by SAL administration.

Indexed as

AnimalsBrain Injuries, TraumaticCinnamatesDisease Models, AnimalEncephalitisEndoplasmic Reticulum StressFrontal LobeImpulsive BehaviorMaleNeuroprotective AgentsOxidative StressRatsRats, Sprague-DawleyThioureaCinnamatesNeuroprotective AgentssalubrinalThioureaEndoplasmic reticulum stressImpulsive-like behaviorNeuroinflammationOxidative stressTraumatic brain injury

Identifiers

PMID27131989
PMCPMC5578618
OpenAlexW2344907496

What OpenQuestion holds

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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.