Evidence map›Paper›PMID 24519543›Full record

ArticleNeurochemical research2014

N-acetylcysteine and selenium modulate oxidative stress, antioxidant vitamin and cytokine values in traumatic brain injury-induced rats.

Nilgün Senol, Mustafa Nazıroğlu, Vehbi Yürüker

Abstract read
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In one paragraph

Article in Neurochemical research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
8.3field-weighted citation impact, top 2% 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

33 citing papers in PubMed, 70 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. N-Acetylcysteine and Probenecid Adjuvant Therapy for Traumatic Brain Injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023
    Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Antioxidant Therapies in Traumatic Brain Injury.Antioxidants (Basel, Switzerland) · 2020
    Review
  13. Ferroptosis in Acute Central Nervous System Injuries: The Future Direction?Frontiers in cell and developmental biology · 2020
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Early Administration of Selenium in Patients with Acute Traumatic Brain Injury: A Randomized Double-blinded Controlled Trial.Indian journal of critical care medicine : peer-reviewed, official publication of Indian Society of Critical Care Medicine · 2017
    Article
  20. Article
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

3 authors at 2 institutions in 2 countries.

Nilgün SenolDepartment of Neurosurgery, Faculty of Medicine, University of Suleyman Demirel, Isparta, Turkey.
Mustafa Nazıroğlu
Vehbi Yürüker
Süleyman Demirel University · TRSuleyman Demirel University · KZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It has been suggested that oxidative stress plays an important role in the pathophysiology of traumatic brain injury (TBI). N-acetylcysteine (NAC) and selenium (Se) display neuroprotective activities mediated at least in part by their antioxidant and anti-inflammatory properties although there is no report on oxidative stress, antioxidant vitamin, interleukin-1 beta (IL)-1β and IL-4 levels in brain and blood of TBI-induced rats. We investigated effects of NAC and Se administration on physical injury-induced brain toxicity in rats. Thirty-six male Sprague-Dawley rats were equally divided into four groups. First and second groups were used as control and TBI groups, respectively. NAC and Se were administrated to rats constituting third and forth groups at 1, 24, 48 and 72 h after TBI induction, respectively. At the end of 72 h, plasma, erythrocytes and brain cortex samples were taken. TBI resulted in significant increase in brain cortex, erythrocytes and plasma lipid peroxidation, total oxidant status (TOS) in brain cortex, and plasma IL-1β values although brain cortex vitamin A, β-carotene, vitamin C, vitamin E, reduced glutathione (GSH) and total antioxidant status (TAS) values, and plasma vitamin E concentrations, plasma IL-4 level and brain cortex and erythrocyte glutathione peroxidase (GSH-Px) activities decreased by TBI. The lipid peroxidation and IL-1β values were decreased by NAC and Se treatments. Plasma IL-4, brain cortex GSH, TAS, vitamin C and vitamin E values were increased by NAC and Se treatments although the brain cortex vitamin A and erythrocyte GSH-Px values were increased through NAC only. In conclusion, NAC and Se caused protective effects on the TBI-induced oxidative brain injury and interleukin production by inhibiting free radical production, regulation of cytokine-dependent processes and supporting antioxidant redox system.

Indexed as

AcetylcysteineAnimalsAntioxidantsBrain InjuriesCytokinesMaleNeuroprotective AgentsOxidative StressRandom AllocationRatsRats, Sprague-DawleySeleniumVitamin AAcetylcysteineAntioxidantsCytokinesNeuroprotective AgentsSeleniumVitamin A

Identifiers

PMID24519543
OpenAlexW2074447472

What OpenQuestion holds

Textmetadata
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.