Evidence map›Paper›PMID 28822838›Full record

ArticleExperimental neurology2017

Scavenging reactive oxygen species inhibits status epilepticus-induced neuroinflammation.

Pallavi B McElroy, Li-Ping Liang, Brian J Day, Manisha Patel

Open access · greenAbstract read
In one paragraph

Article in Experimental neurology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

47 citing papers in PubMed, 93 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review
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

4 authors at 2 institutions in 1 country.

Pallavi B McElroyDepartment of Pharmaceutical Sciences, University of Colorado Denver, Aurora, CO, United States.
Li-Ping LiangDepartment of Pharmaceutical Sciences, University of Colorado Denver, Aurora, CO, United States.
Brian J DayDepartment of Pharmaceutical Sciences, University of Colorado Denver, Aurora, CO, United States; Department of Medicine, National Jewish Health, Denver, CO, United States.
Manisha PatelDepartment of Pharmaceutical Sciences, University of Colorado Denver, Aurora, CO, United States. Electronic address: manisha.patel@ucdenver.edu.
University of Colorado Denver · USNational Jewish Health · US

Funding

ZEBRAFISH TRANSGENIC CORE - ROCKY MOUNTAIN NEUROLOGICAL DISORDERS CORE CENTERP30NS048154 · NINDS · UNIVERSITY OF COLORADO DENVER · PI RIBERA, ANGELES BADELL · 2004 to 2020
$10.1M
SUPEROXIDE RADICALS IN SEIZURE-INDUCED NEURONAL DEATHR01NS039587 · NINDS · UNIVERSITY OF COLORADO DENVER · PI PATEL, MANISHA N · 2000 to 2019
$5.9M
Neuroprotective effects of AEOL 10150 against organophosphate toxicityU01NS083422 · NINDS · UNIVERSITY OF COLORADO DENVER · PI PATEL, MANISHA N · 2013 to 2017
$4.3M
Redox Control of Seizure-Induced Neuroinflammation.R01NS086423 · NINDS · UNIVERSITY OF COLORADO DENVER · PI PATEL, MANISHA N · 2013 to 2022
$3.0M
NINDS NIH HHS P30 NS048154NINDS NIH HHS R01 NS039587NINDS NIH HHS R01 NS086423NINDS NIH HHS U01 NS083422
6 · The paper itself

Abstract

Inflammation has been identified as an important mediator of seizures and epileptogenesis. Understanding the mechanisms underlying seizure-induced neuroinflammation could lead to the development of novel therapies for the epilepsies. Reactive oxygen species (ROS) are recognized as mediators of seizure-induced neuronal damage and are known to increase in models of epilepsies. ROS are also known to contribute to inflammation in several disease states. We hypothesized that ROS are key modulators of neuroinflammation i.e. pro-inflammatory cytokine production and microglial activation in acquired epilepsy. The role of ROS in modulating seizure-induced neuroinflammation was investigated in the pilocarpine model of temporal lobe epilepsy (TLE). Pilocarpine-induced status epilepticus (SE) resulted in a time-dependent increase in pro-inflammatory cytokine production in the hippocampus and piriform cortex. Scavenging ROS with a small-molecule catalytic antioxidant decreased SE-induced pro-inflammatory cytokine production and microglial activation, suggesting that ROS contribute to SE-induced neuroinflammation. Scavenging ROS also attenuated phosphorylation of ribosomal protein S6, the downstream target of the mammalian target of rapamycin (mTOR) pathway indicating that this pathway might provide one mechanistic link between SE-induced ROS production and inflammation. Together, these results demonstrate that ROS contribute to SE-induced cytokine production and antioxidant treatment may offer a novel approach to control neuroinflammation in epilepsy.

Indexed as

AnimalsAntioxidantsHippocampusInflammationInflammation MediatorsMaleRandom AllocationRatsRats, Sprague-DawleyReactive Oxygen SpeciesStatus EpilepticusAntioxidantsInflammation MediatorsReactive Oxygen SpeciesAntioxidantCytokineEpilepsyMammalian target of rapamycinMicroglial activationNeuroinflammationPilocarpineReactive oxygen species

Identifiers

PMID28822838
PMCPMC5658247
OpenAlexW2748480491

What OpenQuestion holds

Textmetadata
LicenceTDM
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.