Evidence map›Paper›PMID 27872485›Full record

ArticleScientific reports2016

The neuroprotective action of dexmedetomidine on apoptosis, calcium entry and oxidative stress in cerebral ischemia-induced rats: Contribution of TRPM2 and TRPV1 channels.

Hatice Akpınar, Mustafa Nazıroğlu, İshak Suat Övey, Bilal Çiğ, Orhan Akpınar

Erratum issued Registry-linked trialOpen access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. It is linked to trial NCT03513757 (An Observer-blinded Randomized Study of Propofol Infusion vs Bolus Dexmedetomidine and Propofol Sedation for Pediatric Magnetic Resonance Imaging), which is not on this map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
7.1field-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.

NCT03513757 phase4completednot on this mapstarted 2018, after this paper: background citation

An Observer-blinded Randomized Study of Propofol Infusion vs Bolus Dexmedetomidine and Propofol Sedation for Pediatric Magnetic Resonance Imaging

TypeinterventionalSponsorMedical College of WisconsinRan2018 to 2018Enrolled40ConditionsHeadache, Tumor, Seizure Disorder, NeurofibromatosesArmspropofol, Dexmedetomidine, Glycopyrrolate, Lidocaine 1% Injectable Solution, Nitrous Oxide
3 · Its place in the literature

Who cites it

50 citing papers in PubMed, 104 citations in OpenAlex.

  1. Trial
  2. Article
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  5. Anesthetics in pathological cerebrovascular conditions.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2025
    Review
  6. Review
  7. Review
  8. Article
  9. TLR4 induced TRPM2 mediated neuropathic pain.Frontiers in pharmacology · 2024
    Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Hatice AkpınarUnit of Anesthesiology and Reanimation, Department of Oral and Maxillofacial Surgery, Faculty of Dentistry, University of Süleyman Demirel, Isparta, Turkey.
Mustafa NazıroğluDepartment of Neuroscience, Institute of Health Science, University of Süleyman Demirel, Isparta, Turkey.
İshak Suat ÖveyDepartment of Neuroscience, Institute of Health Science, University of Süleyman Demirel, Isparta, Turkey.
Bilal ÇiğDepartment of Neuroscience, Institute of Health Science, University of Süleyman Demirel, Isparta, Turkey.
Orhan AkpınarUnit of Microbiology, Department of Oral and Maxillofacial Surgery, Faculty of Dentistry, University of Süleyman Demirel, Isparta, Turkey.
Süleyman Demirel University · TR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dexmedetomidine (DEX) may act as an antioxidant through regulation of TRPM2 and TRPV1 channel activations in the neurons by reducing cerebral ischemia-induced oxidative stress and apoptosis. The neuroprotective roles of DEX were tested on cerebral ischemia (ISC) in the cultures of rat primary hippocampal and DRG neurons. Fifty-six rats were divided into five groups. A placebo was given to control, sham control, and ISC groups, respectively. In the third group, ISC was induced. The DEX and ISC+DEX groups received intraperitoneal DEX (40 μg/kg) 3, 24, and 48 hours after ISC induction. DEX effectively reversed capsaicin and cumene hydroperoxide/ADP-ribose-induced TRPV1 and TRPM2 densities and cytosolic calcium ion accumulation in the neurons, respectively. In addition, DEX completely reduced ISC-induced oxidative toxicity and apoptosis through intracellular reactive oxygen species production and depolarization of mitochondrial membrane. The DEX and ISC+DEX treatments also decreased the expression levels of caspase 3, caspase 9, and poly (ADP-ribose) polymerase in the hippocampus and DRG. In conclusion, the current results are the first to demonstrate the molecular level effects of DEX on TRPM2 and TRPV1 activation. Therefore, DEX can have remarkable neuroprotective impairment effects in the hippocampus and DRG of ISC-induced rats.

Indexed as

AnimalsApoptosisBrain DiseasesCalciumDexmedetomidineGanglia, SpinalHippocampusMaleNeuronsNeuroprotective AgentsOxidative StressRatsRats, WistarReperfusion InjuryTRPM Cation ChannelsTRPV Cation ChannelsCalciumDexmedetomidineNeuroprotective AgentsTrpm2 protein, ratTRPM Cation ChannelsTrpv1 protein, ratTRPV Cation Channels

Identifiers

PMID27872485
PMCPMC5131653
OpenAlexW2549863851

What OpenQuestion holds

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Registered trials

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.