Evidence map›Paper›PMID 24460643›Full record

ArticleJournal of neuroinflammation2014

Protection of ischemic post conditioning against transient focal ischemia-induced brain damage is associated with inhibition of neuroinflammation via modulation of TLR2 and TLR4 pathways.

Ying Wang, Pengfei Ge, Li Yang, Chunyun Wu, Hao Zha, Tianfei Luo, Yuhong Zhu

Registry-linked trialOpen access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03176823 (Remote Ischemic Conditioning as a Treatment for Traumatic Brain Injury), which is not on this map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
4.4field-weighted citation impact, top 5% 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.

NCT03176823 nacompletednot on this mapstarted 2019, after this paper: background citation

Remote Ischemic Conditioning as a Treatment for Traumatic Brain Injury: a Prospective Randomized Controlled Trial.

TypeinterventionalSponsorUnity Health TorontoRan2019 to 2024Enrolled44ConditionsTraumatic Brain Injury, Trauma, Nervous System, Reperfusion Injury, Ischemia, BrainArmsCellAegis Technologies autoRIC device, Best Practice Management of Traumatic Brain Injury
3 · Its place in the literature

Who cites it

24 citing papers in PubMed, 58 citations in OpenAlex.

  1. Review
  2. Review
  3. Delayed COCNS neuroscience & therapeutics · 2023
    Article
  4. The Role of ncRNAs in Cardiac Infarction and Regeneration.Journal of cardiovascular development and disease · 2023
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Nutrients · 2021
    Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
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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

7 authors at 2 institutions in 1 country.

Ying Wang
Pengfei Ge
Li Yang
Chunyun Wu
Hao Zha
Tianfei Luo
Yuhong ZhuDepartment of Neurology, Second Affiliated Hospital of Kunming Medical University, Kunming 650031, China. yuhong_lilin@aliyun.com.
Kunming Medical University · CNJilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeIschemic postconditioning has been demonstrated to be a protective procedure to brain damage caused by transient focal ischemia/reperfusion. However, it is elusive whether the protection of postconditioning against brain damage and neuroinflammation is via regulating TLR2 and TLR4 pathways. In the present study, we examined the protection of ischemic postconditioning performed immediately prior to the recovery of cerebral blood supply on brain damage caused by various duration of ischemia and tested the hypothesis that its protection is via inhibition of neuroinflammation by modulating TLR2/TLR4 pathways.

methodsBrain damage in rats was induced by using the middle cerebral artery occlusion (MCAO) model. Ischemic postconditioning consisting of fivecycles of ten seconds of ischemia and reperfusion was performed immediately following theischemic episode Theduration of administration of ischemic postconditioning was examined by comparing its effects on infarction volume, cerebral edema and neurological function in 2, 3, 4, 4.5and 6 hour ischemia groups. The protective mechanism of ischemic postconditioning was investigated by comparing its effects on apoptosis, production of the neurotoxic cytokine IL-1β and the transcription and expression of TLR2, TLR4 and IRAK4 in the 2 and 4.5 hour ischemia groups.

resultsIschemic postconditioning significantly attenuated cerebral infarction, cerebral edema and neurological dysfunction in ischemia groups of up to 4 hours duration, but not in 4.5and 6 hour ischemia groups. It also inhibited apoptosis, production of IL-1β, abnormal transcription and expression of TLR2, TLR4 and IRAK4 in the 2 hour ischemia group, but not in the 4.5 hour ischemia group.

conclusionsIschemic postconditioning protected brain damage caused by 2, 3 and 4 hours of ischemia, but not by 4.5 and 6 hours of ischemia. The protection of ischemic postconditioning is associated with its inhibition of neuroinflammation via inhibition of TLR2 and TLR4 pathways.

Indexed as

Ischemic PostconditioningAnimalsApoptosisBrain EdemaBrain InfarctionBrain InjuriesCytokinesDisease Models, AnimalEncephalitisGene Expression RegulationHumansInfarction, Middle Cerebral ArteryMaleNeurologic ExaminationRatsRats, Sprague-DawleyCytokinesTlr2 protein, ratTlr4 protein, ratToll-Like Receptor 2Toll-Like Receptor 4

Identifiers

PMID24460643
PMCPMC3908918
OpenAlexW2101350212

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.