Evidence map›Paper›PMID 26861954›Full record

ArticleNeurotoxicity research2016

N-Acetylcysteine and Ceftriaxone as Preconditioning Strategies in Focal Brain Ischemia: Influence on Glutamate Transporters Expression.

Weronika Krzyzanowska, Bartosz Pomierny, Boguslawa Budziszewska, Malgorzata Filip, Joanna Pera

Open access · hybridAbstract read
In one paragraph

Article in Neurotoxicity research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.5field-weighted citation impact, top 8% 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

19 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Review
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  4. Cysteine induces mitochondrial reductive stress in glioblastoma through hydrogen peroxide production.Proceedings of the National Academy of Sciences of the United States of America · 2024
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  8. The Slow-Releasing and Mitochondria-Targeted Hydrogen Sulfide (HInternational journal of molecular sciences · 2021
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  15. Article
  16. Intervention action of total flavonoids from root ofSaudi journal of biological sciences · 2017
    Article
  17. Article
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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

5 authors at 1 institution in 1 country.

Weronika KrzyzanowskaDepartment of Biochemical Toxicology, Faculty of Pharmacy, Jagiellonian University, Medical College, Medyczna 9, 30-688, Krakow, Poland.
Bartosz PomiernyDepartment of Biochemical Toxicology, Faculty of Pharmacy, Jagiellonian University, Medical College, Medyczna 9, 30-688, Krakow, Poland. bartosz.pomierny@uj.edu.pl.
Boguslawa BudziszewskaDepartment of Biochemical Toxicology, Faculty of Pharmacy, Jagiellonian University, Medical College, Medyczna 9, 30-688, Krakow, Poland.
Malgorzata FilipDepartment of Toxicology, Faculty of Pharmacy, Jagiellonian University, Medical College, Medyczna 9, 30-688, Krakow, Poland.
Joanna PeraDepartment of Neurology, Jagiellonian University, Medical College, Botaniczna 3, 31-503, Krakow, Poland.
Jagiellonian University · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glutamate (Glu) plays a key role in excitotoxicity-related injury in cerebral ischemia. In the brain, Glu homeostasis depends on Glu transporters, including the excitatory amino acid transporters and the cysteine/Glu antiporter (xc-). We hypothesized that drugs acting on Glu transporters, such as ceftriaxone (CEF, 200 mg/kg, i.p.) and N-acetylcysteine (NAC, 150 mg/kg, i.p.), administered repeatedly for 5 days before focal cerebral ischemia in rats and induced by a 90-min middle cerebral artery occlusion (MCAO), may induce brain tolerance to ischemia. We compared the effects of these drugs on brain infarct volume, neurological deficits and the mRNA and protein expression of the Glu transporter-1 (GLT-1) and xc- with the effects of ischemic preconditioning and chemical preconditioning using 3-nitropropionic acid. Administration of CEF and NAC significantly reduced infarct size and neurological deficits caused by a 90-min MCAO. These beneficial effects were accompanied by changes in GLT-1 expression caused by a 90-min MCAO at both the mRNA and protein levels in the frontal cortex, hippocampus, and dorsal striatum. Thus, the results of this study suggest that the regulation of GLT-1 and xc- plays a role in the development of cerebral tolerance to ischemia and that this regulation may be a novel approach in the therapy of brain ischemia.

Indexed as

AcetylcysteineAnalysis of VarianceAnimalsBrainBrain EdemaBrain InfarctionCeftriaxoneDisease Models, AnimalDrug Administration ScheduleEnzyme-Linked Immunosorbent AssayExcitatory Amino Acid Transporter 2Gene Expression RegulationInfarction, Middle Cerebral ArteryMaleNervous System DiseasesNeuroprotective AgentsAcetylcysteineCeftriaxoneExcitatory Amino Acid Transporter 2Neuroprotective AgentsRNA, MessengerSlc1a2 protein, ratBrain ischemiaBrain preconditioningCeftriaxoneN-acetylcysteineNeuroprotection

Identifiers

PMID26861954
PMCPMC4820483
OpenAlexW2265508213

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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.