Evidence map›Paper›PMID 21277352›Full record

ArticleNeuroscience2011

Volatile anesthetic post-treatment induces protection via inhibition of glycogen synthase kinase 3β in human neuron-like cells.

D Lin, G Li, Z Zuo

Abstract read
In one paragraph

Article in Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
4.0field-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

24 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
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  4. Review
  5. Autophagy Induced by Oxygen-Glucose Deprivation Mediates the Injury to the Neurovascular Unit.Medical science monitor : international medical journal of experimental and clinical research · 2019
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  6. Article
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  9. The choice of general anesthetics may not affect neuroinflammation and impairment of learning and memory after surgery in elderly rats.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2015
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  16. Review
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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

3 authors at 1 institution in 2 countries.

D LinDepartment of Anesthesiology, University of Virginia, Charlottesville, VA 22908, USA.
G Li
Z Zuo
University of Virginia · US

Funding

Volatile anesthetic modulation of glutamate transportersR01GM065211 · NIGMS · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI ZUO, ZHIYI · 2003 to 2011
$2.6M
NIGMS NIH HHS R01 GM065211
6 · The paper itself

Abstract

Application of the volatile anesthetic isoflurane during the early phase of reperfusion reduces ischemic heart and brain injury (anesthetic post-conditioning). We hypothesize that inhibition of glycogen synthase kinase 3β (GSK3β), a protein whose activation can lead to cell death, participates in anesthetic post-conditioning-induced neuroprotection. SH-SY5Y cells, a human neuroblastoma cell line, were induced by retinoic acid to differentiate into terminal neuron-like cells. The cells were then subjected to a 1-h oxygen-glucose deprivation (OGD), a condition to simulate ischemia in vitro, and a 20-h simulated reperfusion. Isoflurane, sevoflurane or desflurane, three commonly used volatile anesthetics, were applied for 1 h during the early phase of simulated reperfusion. Cell injury was quantified by lactate dehydrogenase (LDH) release. Phospho-GSK3β at Ser9 and total GSK3β were quantified at 1 or 3 h after the OGD. OGD increased LDH release, suggesting that OGD induced cell injury. Post-treatment with isoflurane, sevoflurane or desflurane reduced this cell injury. This protection was apparent when 2% isoflurane was applied within 1 h after the onset of reperfusion. Isoflurane post-treatment also significantly increased the phosphorylation of GSK3β at Ser9 at 1 h after the OGD. GSK3β inhibitors reduced OGD and simulated reperfusion-induced LDH release. The combination of GSK3β inhibitors and isoflurane post-conditioning did not cause a greater protection than isoflurane post-conditioning alone. These results suggest that volatile anesthetic post-conditioning reduces OGD and simulated reperfusion-induced cell injury. Since phospho-GSK3β at Ser9 decreases GSK3β activity, our results suggest that volatile anesthetic post-conditioning in human neuron-like cells may be mediated by GSK3β inhibition.

Indexed as

Anesthetics, InhalationBlotting, WesternCell LineDesfluraneEnzyme InhibitorsGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHumansIschemic PostconditioningIsofluraneMethyl EthersNeuronsNeuroprotective AgentsSevofluraneAnesthetics, InhalationDesfluraneEnzyme InhibitorsGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGSK3B protein, humanIsofluraneMethyl EthersNeuroprotective AgentsSevoflurane

Identifiers

PMID21277352
PMCPMC3059391
OpenAlexW2082311917

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.