Evidence map›Paper›PMID 33201349›Full record

ArticleInflammopharmacology2021

Donepezil attenuates injury following ischaemic stroke by stimulation of neurogenesis, angiogenesis, and inhibition of inflammation and apoptosis.

Arian Madani Neishaboori, Solmaz Nasseri Maleki, Mahdi Saberi Pirouz, Sara Golmohammadi, Donya Nazarinia, Nahid Aboutaleb

Abstract read
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In one paragraph

Article in Inflammopharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 24% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Frontiers in pharmacology · 2022
    Article
  9. Article
  10. Article
  11. Article
  12. Topical Donepezil for Cholinergic Modulation in Chronic Wound Repair.Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society
    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

6 authors at 2 institutions in 1 country.

Arian Madani Neishaboori *Physiology Research Center, Iran University of Medical Sciences, Tehran, Iran.
Solmaz Nasseri Maleki *Physiology Research Center, Iran University of Medical Sciences, Tehran, Iran.
Mahdi Saberi PirouzPhysiology Research Center, Iran University of Medical Sciences, Tehran, Iran.
Sara GolmohammadiPhysiology Research Center, Iran University of Medical Sciences, Tehran, Iran.
Donya NazariniaDepartment of Physiology, School of Paramedical Sciences, Dezful University of Medical Sciences, Dezful, Iran.
Nahid AboutalebPhysiology Research Center, Iran University of Medical Sciences, Tehran, Iran. Aboutaleb.n@iums.ac.ir.ORCID http://orcid.org/0000-0002-7514-5939
Iran University of Medical Sciences · IRDezful University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Donepezil has proven to be an effective drug to reduce neuronal death and subsequently injury in neurodegenerative diseases. The current study evaluated the neuroprotective effects of donepezil in a rat model of ischaemic stroke and explored possible mechanisms which by this drug may reduce cell death. Temporary middle cerebral artery occlusion (tMCAO) was exerted for 45 min to induce ischaemic stroke. The animals were assigned into five groups: sham, control, and three groups treated with different doses of donepezil. Donepezil was intraperitoneally (IP) injected 4 h after reperfusion for 10 consecutive days. Infarct size was determined using TTC staining. The expression of proteins was evaluated using immunohistochemistry assays. Compared with the control group, infarct size was significantly reduced in tMCAO rats treated with different doses of donepezil. Moreover, our results showed significant decreased expression levels of apoptotic markers and pro-inflammatory mediators after treatment with different doses of donepezil for 10 days (P < 0.05). Likewise, significant increase of brain-derived neurotrophic factor (BDNF) and peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) proteins were found in tMCAO rats treated with donepezil compared with the control group (P < 0.05). Collectively, our findings show the validity of donepezil as a new therapeutic agent for attenuation of injury following ischaemic stroke through attenuation of inflammation and improvement of mitochondrial function, neurogenesis, and angiogenesis.

Indexed as

Angiogenesis Inducing AgentsAnimalsApoptosisDonepezilDose-Response Relationship, DrugInfarction, Middle Cerebral ArteryInflammationIschemic StrokeMaleMitochondriaNeurogenesisNeuroprotective AgentsRatsRats, WistarAngiogenesis Inducing AgentsDonepezilNeuroprotective AgentsAngiogenesisApoptosisBDNF proteinDonepezilFocal cerebral ischaemiaMitochondrial function

Identifiers

PMID33201349
OpenAlexW3105168804

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.