Evidence map›Paper›PMID 38939996›Full record

ArticleCurrent medicinal chemistry2025

Europinidin Attenuates Methamphetamine-induced Learning and Memory Impairments and Hippocampal Alterations in Rodents: Based on Molecular Docking through a Mechanism of Neuromodulatory Cytokines/ Caspases-3/ CREB/BDNF Pathway.

Ryan A Sheikh, Muhammad Afzal, Fahad A Al-Abbasi, Hussam A Bukhari, Naif A R Almalki, May M Alqurashi, Faisal Imam, Nadeem Sayyed, Imran Kazmi

Abstract read
PubMed Publisher
In one paragraph

Article in Current medicinal chemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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. Article
  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

9 authors.

Ryan A SheikhDepartment of Biochemistry, Faculty of Sciences, King Abdulaziz University, Jeddah, 21589, Saudi Arabia.
Muhammad AfzalDepartment of Pharmaceutical Sciences, Pharmacy Program, Batterjee Medical College, P.O. Box 6231, Jeddah, 21442, Saudi Arabia.
Fahad A Al-AbbasiDepartment of Biochemistry, Faculty of Sciences, King Abdulaziz University, Jeddah, 21589, Saudi Arabia.
Hussam A BukhariDepartment of Pathology, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia.
Naif A R AlmalkiDepartment of Biochemistry, Faculty of Sciences, King Abdulaziz University, Jeddah, 21589, Saudi Arabia.
May M AlqurashiDepartment of Biochemistry, Faculty of Sciences, King Abdulaziz University, Jeddah, 21589, Saudi Arabia.
Faisal ImamDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, P.O. Box 2457, Riyadh, 11451, Saudi Arabia.
Nadeem SayyedSchool of Pharmacy, Glocal University, Saharanpur, 247121, India.
Imran KazmiDepartment of Biochemistry, Faculty of Sciences, King Abdulaziz University, Jeddah, 21589, Saudi Arabia.

Funding

King Saud University, Riyadh, Saudi Arabia RSPD2024R939
6 · The paper itself

Abstract

backgroundMethamphetamine (MA) is well recognized as a psychostimulant that can cause neurotoxicity and neurodegeneration, which is associated with cognitive decline, has been confirmed experimentally.

objectiveThe research aimed to investigate the neuroprotective properties of europinidin (Eu) in rodents affected by methamphetamine (MA)-induced cognitive impairments and hippocampal alterations. This was achieved by inhibiting lipid peroxidation and pro-inflammatory markers.

methodsRats were exposed to cognitive impairment produced by MA. The Morris water maze (MWM) is utilized to evaluate behavioral parameters. Biochemical tests were conducted on malondialdehyde (MDA), catalase (CAT), interleukins-1β (IL-1β), reduced glutathione (GSH), tumor necrosis factor-α (TNF-α), superoxide dismutase (SOD), and the expression of neurotransmitters (Norepinephrine [NE], dopamine [DA], glutamate, and gamma-aminobutyric acid [GABA]) as well as cAMP response element- binding protein (CREB), IL-6, brain-derived neurotrophic factor (BDNF), and caspase 3 proteins. An investigation was carried out using docking methodology to ascertain whether Eu interacts with relevant molecular targets.

resultsSignificant decline in the transfer latency and there were significant changes in the amount of SOD, GSH, CAT, and MDA and alterations in levels of IL-6, IL-1β, CREB, TNF-α, BDNF, and Caspase 3 proteins expression. Furthermore, considerably restored level of neurotransmitters (NE, DA, Glutamate, and GABA) were observed in the Eu-treated rats compared to the MA-induced rats. Eu had a favorable affinity towards BDNF with docking scores of -9.486 kcal/mol.

conclusionThe experiment found that administering Eu to rats improved cognitive abilities by changing antioxidant enzymes, reducing cytokines, and modifying neurotransmitter levels, compared to rats in the control group treated with MA.

Indexed as

HippocampusMemory DisordersMethamphetamineMolecular Docking SimulationNeuroprotective AgentsAnimalsBrain-Derived Neurotrophic FactorCaspase 3Cyclic AMP Response Element-Binding ProteinCytokinesMaleMaze LearningRatsSignal TransductionBdnf protein, ratBrain-Derived Neurotrophic FactorCaspase 3Cyclic AMP Response Element-Binding ProteinCytokinesMethamphetamineNeuroprotective Agentseuropinidinglutamate.methamphetamineNeuroinflammatory cytokinesneuroprotectiveoxidative stress

Identifiers

PMID38939996

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.