Evidence map›Paper›PMID 30083945›Full record

ArticleNaunyn-Schmiedeberg's archives of pharmacology2018

Vinpocetine halts ketamine-induced schizophrenia-like deficits in rats: impact on BDNF and GSK-3β/β-catenin pathway.

Hebatalla I Ahmed, Somaia A Abdel-Sattar, Heba S Zaky

Abstract read
PubMed Publisher
In one paragraph

Article in Naunyn-Schmiedeberg's archives of pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
0.8field-weighted citation impact, top 32% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. The relationship between neurodevelopmental disorders (NDDs) and NLRP3 inflammasome.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Cognitive Deficit in Schizophrenia: From Etiology to Novel Treatments.International journal of molecular sciences · 2021
    Review
  20. 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

3 authors at 1 institution in 1 country.

Hebatalla I AhmedDepartment of Pharmacology and Toxicology, Faculty of Pharmacy (Girls), Al-Azhar University, Cairo, 11754, Egypt. hebatalla123@yahoo.com.ORCID 0000-0001-8634-6210
Somaia A Abdel-SattarDepartment of Pharmacology and Toxicology, Faculty of Pharmacy (Girls), Al-Azhar University, Cairo, 11754, Egypt.
Heba S ZakyDepartment of Pharmacology and Toxicology, Faculty of Pharmacy (Girls), Al-Azhar University, Cairo, 11754, Egypt.
Al-Azhar University · EG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

There are increasing evidences supporting the involvement of oxidative stress and neuroinflammation in schizophrenia. Vinpocetine, a nootropic phosphodiesterase-1 inhibitor, was proven to possess anti-oxidant and anti-inflammatory potentials. This research aimed to reveal the likely protective features of vinpocetine against ketamine-induced schizophrenia-like deficits in rats. Additionally, the probable mechanisms contributing to this neuroprotection were also elucidated. Vinpocetine was given (20 mg/kg, i.p.) once a day for 14 days commencing 7 days before administrating ketamine (25 mg/kg i.p.). Risperidone was applied as a reference antipsychotic. Vinpocetine pre-treatment revealed a marked amendment in the hyperlocomotion, anxiety, and short-term memory deficits induced by ketamine in rats. In rats' hippocampus, ketamine induced a drastic increase in tissue levels of dopamine, lipid peroxidation, and pro-inflammatory cytokines along with a significant decrease in glutamate, GABA, SOD, and total anti-oxidant capacity. Also, ketamine induced a reduced level of BDNF together with the potentiation of GSK-3β/β-catenin pathway that led to the destruction of β-catenin. Pre-treatment of ketamine-challenged animals with vinpocetine significantly attenuated oxidative stress, inflammation, and neurotransmitter alterations. Vinpocetine also elevated BDNF expression and prevented ketamine-induced stimulation of the GSK-3β/β-catenin signaling. This research presents enlightenments into the role of vinpocetine in schizophrenia. This role may be accomplished through its effect on oxidative stress, inflammation as well as modulating BDNF and the GSK-3β/β-catenin pathway.

Indexed as

AnimalsAntipsychotic AgentsBehavior, Animalbeta CateninBrain-Derived Neurotrophic FactorGlycogen Synthase Kinase 3 betaHippocampusKetamineMaleMalondialdehydeOxidative StressRats, Sprague-DawleySchizophreniaSignal TransductionVinca AlkaloidsAntipsychotic AgentsBdnf protein, ratbeta CateninBrain-Derived Neurotrophic FactorCtnnb1 protein, ratGlycogen Synthase Kinase 3 betaKetamineMalondialdehydeVinca AlkaloidsvinpocetineBrain-derived neurotrophic factorGlycogen synthase kinase-3βRatsSchizophreniaVinpocetineβ-Catenin

Identifiers

PMID30083945
OpenAlexW2885961754

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.