Evidence map›Paper›PMID 23943518›Full record

ArticleMolecular neurobiology2014

Glycogen synthase kinase-3β is involved in electroacupuncture pretreatment via the cannabinoid CB1 receptor in ischemic stroke.

Haidong Wei, Xi Yao, Lifang Yang, Shiquan Wang, Fan Guo, Heng Zhou, Giovanni Marsicano, Qiang Wang, Lize Xiong

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
11.8field-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

30 citing papers in PubMed, 43 citations in OpenAlex.

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  19. Signal Transduction Pathways of Acupuncture for Treating Some Nervous System Diseases.Evidence-based complementary and alternative medicine : eCAM · 2019
    Review
  20. Acupuncture and neuroregeneration in ischemic stroke.Neural regeneration research · 2018
    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

9 authors at 4 institutions in 2 countries.

Haidong WeiDepartment of Anesthesiology, Xijing Hospital, The Fourth Military Medical University, Xi'an, 710032, Shaanxi, China.
Xi Yao
Lifang Yang
Shiquan Wang
Fan Guo
Heng Zhou
Giovanni Marsicano
Qiang Wang
Lize Xiong
Xijing Hospital · CNAir Force Medical University · CNNeurocentre Magendie · FRThe First Affiliated Hospital, Sun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We have previously shown that electroacupuncture (EA) pretreatment produces neuroprotective effects, which were mediated through an endocannabinoid signal transduction mechanism. Herein, we have studied the possible contribution of the phosphorylated form of glycogen synthase kinase-3β (GSK-3β) in EA pretreatment-induced neuroprotection via the cannabinoid CB1 receptor (CB1R). Focal transient cerebral ischemia was induced by middle cerebral artery occlusion in rats. Phosphorylation of GSK-3β at Ser-9 [p-GSK-3β (Ser-9)] was evaluated in the penumbra tissue following reperfusion. Infarct size and neurological score were assessed in the presence of either PI3K inhibitors or a GSK-3β inhibitor 72 h after reperfusion. Cellular apoptosis was evidenced by TUNEL staining and determination of the Bax/Bcl-2 ratio 24 h after reperfusion. The present study showed that EA pretreatment increased p-GSK-3β(Ser-9) 2 h after reperfusion in the ipsilateral penumbra. Augmented phosphorylation of GSK-3β induced similar neuroprotective effects as did EA pretreatment. By contrast, inhibition of PI3K dampened the levels of p-GSK-3β(Ser-9), and reversed not only the neuroprotective effect but also the anti-apoptotic effect following EA pretreatment. Regulation of GSK-3β by EA pretreatment was abolished following treatment with a CB1R antagonist and CB1R knockdown, whereas two CB1R agonists enhanced the phosphorylation of GSK-3β. Therefore we conclude that EA pretreatment protects against cerebral ischemia/reperfusion injury through CB1R-mediated phosphorylation of GSK-3β.

Indexed as

AndrostadienesAnimalsBrain IschemiaCannabinoid Receptor AgonistsCannabinoid Receptor AntagonistsChromonesElectroacupunctureGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaInjections, IntraventricularMorpholinesPhosphorylationRandom AllocationRatsRats, Sprague-DawleyReceptor, Cannabinoid, CB12-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-oneAndrostadienesCannabinoid Receptor AgonistsCannabinoid Receptor AntagonistsChromonesGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGsk3b protein, ratMorpholinesReceptor, Cannabinoid, CB1Wortmannin

Identifiers

PMID23943518
OpenAlexW1994447419

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.