Evidence map›Paper›PMID 26186541›Full record

ArticlePloS one2015

Time-Dependent Protection of CB2 Receptor Agonist in Stroke.

Seong-Jin Yu, David Reiner, Hui Shen, Kou-Jen Wu, Qing-Rong Liu, Yun Wang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 2 pooled it
3.4field-weighted citation impact, top 9% 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

41 citing papers in PubMed, 2 syntheses or guidelines pooled it, 67 citations in OpenAlex.

  1. The Effects of Cannabinoids on Ischemic Stroke-Associated Neuroinflammation: A Systematic Review.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025
    Pooled it
  2. Pooled it
  3. Article
  4. Review
  5. Review
  6. Article
  7. Potential of CBD Acting on Cannabinoid Receptors CBInternational journal of molecular sciences · 2024
    Review
  8. Review
  9. Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. Review
  15. Article
  16. Review
  17. Review
  18. Review
  19. 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

6 authors at 2 institutions in 2 countries.

Seong-Jin YuCenter for Neuropsychiatric Research, National Health Research Institutes, Zhunan, Taiwan.
David ReinerNeural Protective and Regeneration Section, National Institute on Drug Abuse, NIH, Baltimore, Maryland, United States of America.
Hui ShenNeural Protective and Regeneration Section, National Institute on Drug Abuse, NIH, Baltimore, Maryland, United States of America.
Kou-Jen WuCenter for Neuropsychiatric Research, National Health Research Institutes, Zhunan, Taiwan.
Qing-Rong LiuNeural Protective and Regeneration Section, National Institute on Drug Abuse, NIH, Baltimore, Maryland, United States of America.
Yun WangCenter for Neuropsychiatric Research, National Health Research Institutes, Zhunan, Taiwan; Neural Protective and Regeneration Section, National Institute on Drug Abuse, NIH, Baltimore, Maryland, United States of America.
National Health Research Institutes · TWNational Institute on Drug Abuse · US

Funding

Intramural NIH HHS
6 · The paper itself

Abstract

Recent studies have indicated that type 2 cannabinoid receptor (CB2R) agonists reduce neurodegeneration after brain injury through anti-inflammatory activity. The purpose of this study was to examine the time-dependent interaction of CB2R and inflammation in stroke brain. Adult male rats were subjected to right middle cerebral artery occlusion (MCAo). CB2R mRNA expression was significantly elevated >20 fold on day 2, peaked >40-fold on day 5, and normalized on day 10 post-stroke. Inflammatory markers IBA1 and TLR4 were significantly upregulated 15 fold until day 5 after MCAo. Because of the delayed upregulation of CB2R and IBA1, we next treated animals daily with CB2R agonist AM1241 or anti-inflammatory PPAR-γ agonist pioglitazone from 2 to 5 days after MCAo. Delayed treatment with pioglitazone significantly reduced abnormal neurological scores and body asymmetry as well as brain infarction in stroke animals. No behavioral improvement or reduction in brain infarction was found in animals receiving AM1241. Pioglitazone, but not AM1241, significantly reduced IBA1 expression in the stroke cortex, suggesting that delayed treatment with AM1241 failed to alter ischemia-mediated IBA-1 upregulation. In contrast, pretreatment with AM1241 significantly reduced brain infarction and neurological deficits. In conclusion, our data support a time-dependent neuroprotection of CB2 agonist in an animal model of stroke. Delayed post- treatment with PPAR-γ agonist induced behavioral recovery and microglial suppression; early treatment with CB2R agonist suppressed neurodegeneration in stroke animals.

Indexed as

NeuroprotectionAnimalsBehavior, AnimalBrain IschemiaCalcium-Binding ProteinsCannabinoid Receptor AgonistsCannabinoidsCerebral CortexGlutamic AcidMaleMicrofilament ProteinsNerve DegenerationNeuronsPioglitazoneRats, Sprague-DawleyReceptor, Cannabinoid, CB1Aif1 protein, ratAM 1241Calcium-Binding ProteinsCannabinoid Receptor AgonistsCannabinoidsGlutamic AcidMicrofilament ProteinsPioglitazoneReceptor, Cannabinoid, CB1Receptor, Cannabinoid, CB2RNA, MessengerThiazolidinedionesToll-Like Receptor 4

Identifiers

PMID26186541
PMCPMC4505877
OpenAlexW1899359459

What OpenQuestion holds

Textmetadata
LicenceCC0
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.