Evidence map›Paper›PMID 31471737›Full record

ArticleMetabolic brain disease2019

Age-related difference in protective effect of early post-conditioning on ischemic brain injury: possible involvement of MAP-2/Synaptophysin role.

Hedayat Samandari, Fatemeh Nabavizadeh, Ghorbangol Ashabi

Abstract read
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In one paragraph

Article in Metabolic brain disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed, 1 pooled it
0.3field-weighted citation impact, top 46% 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

2 citing papers in PubMed, 1 synthesis or guideline pooled it, 4 citations in OpenAlex.

  1. A meta-analysis of remote ischaemic conditioning in experimental stroke.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021
    Pooled it
  2. 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

3 authors at 1 institution in 1 country.

Hedayat SamandariElectrophysiology Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran.
Fatemeh NabavizadehDepartment of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Ghorbangol AshabiDepartment of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. gh-ashabi@tums.ac.ir.
Tehran University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Brain Ischemia/Reperfusion (I/R) injury leads to the failure of the microtubules function and neuronal death. Ischemic post-conditioning is defined as a series of rapid alternating interruptions of blood flow in the first seconds of reperfusion. In the present study, the caspase-3, Microtubule-Associated Protein-2 (MAP-2), Protein Kinase C α (PKCα), c-fos, and synaptophysin were evaluated in the hippocampus of focal I/R post-conditioning model in a time -dependent study in aged and young rats. Adult and aged rats were subjected to right MCAO for 30 min and post-conditioned (10 s) for 3 cycles. Sensory-motor tests were performed, and locomotion and anxiety-like behavior were evaluated. Molecular tests were done by detection kit, RT-PCR, and Western blotting techniques. Ninety-six hours after I/R post-conditioning, neurological signs, locomotion, anxiety-like behavior, and ischemic area were improved in young rats compared to 6 h after I/R post-conditioning (P < 0.001). Caspase-3 activity declined in the hippocampus and cortex of I/R post-conditioned young rats in 96 h after I/R post-conditioning compared with 6 h after I/R post-conditioning (P < 0.001). Also, MAP-2 mRNA, MAP-2 protein level, PKCα, c-fos and synaptophysin protein levels were enhanced during post-conditioning in young rats in 96 h after I/R post-conditioning compared with 6 h after induction of I/R post-conditioning. The results of the present study suggested that, early post-conditioning might be considered as a candidate for therapeutic methods against I/R in the adult animals not aged rats. Moreover, inhibition of cell death in post-conditioned ischemic rats was found to be regulated by some neuroprotective molecules as well as MAP-2 and c-fos in young rats. Graphical abstract Graphical abstract representing the post-conditioning (PC) treatment timeline in adult and old rats.

Indexed as

Age FactorsAnimalsAnxietyBrain IschemiaCaspase 3Cerebral CortexDisease Models, AnimalHippocampusIschemic PostconditioningMaleMicrotubule-Associated ProteinsMotor ActivityProtein Kinase C-alphaProto-Oncogene Proteins c-fosRatsRats, WistarCaspase 3Microtubule-Associated ProteinsProtein Kinase C-alphaProto-Oncogene Proteins c-fosSynaptophysinAgedFocal cerebral ischemiaMAP-2Post-conditioningSynaptophysinYoung

Identifiers

PMID31471737
OpenAlexW2971161739

What OpenQuestion holds

Textmetadata
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.