Evidence map›Paper›PMID 40643651›Full record

ArticleNaunyn-Schmiedeberg's archives of pharmacology2026

Exercise-mediated modulation of hippocampal apoptotic gene expression and behavioral outcomes in methamphetamine-dependent rats.

Shima Ababzadeh, Hamid Reza Salimi, Mohsen Eslami Farsani, Amir Hossein Haghighi, Reihaneh Seyedebrahimi, Donya Heidari, Saeedeh Zare Jalise

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Article in Naunyn-Schmiedeberg's archives of pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

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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

1 citing paper in PubMed.

  1. 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

7 authors.

Shima AbabzadehCellular and Molecular Research Center, Faculty of Medical Sciences, Qom University of Medical Sciences, Qom, Iran.
Hamid Reza SalimiDepartment of Exercise Physiology, Faculty of Sport Sciences, Hakim Sabzevari University, Sabzevar, Iran. h.salimi@tolouemehr.ac.ir.
Mohsen Eslami FarsaniCellular and Molecular Research Center, Faculty of Medical Sciences, Qom University of Medical Sciences, Qom, Iran.
Amir Hossein HaghighiDepartment of Exercise Physiology, Faculty of Sport Sciences, Hakim Sabzevari University, Sabzevar, Iran.
Reihaneh SeyedebrahimiCellular and Molecular Research Center, Faculty of Medical Sciences, Qom University of Medical Sciences, Qom, Iran.
Donya HeidariDepartment of Tissue Engineering & Regenerative Medicine, School of Advanced Technologies in Medicine, Mazandaran University of Medical Sciences, Sari, Iran.
Saeedeh Zare JaliseDepartment of Tissue Engineering and Applied Cell Sciences, Faculty of Medical Sciences, Qom University of Medical Sciences, Qom, Iran.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeMethamphetamine (MA) abuse causes significant neurotoxicity, with limited pharmacological options available to mitigate cognitive deficits. This study investigated whether moderate-intensity aerobic training (MIAT) reduces hippocampal apoptosis and improves cognitive function in MA-exposed rats.

methodsForty male rats were randomly assigned to four groups (Saline, MA, MA + MIAT, and MIAT) and given increasing MA doses (2.5-10 mg/kg) over 23 days. For six consecutive weeks, the rats in the MIAT groups underwent daily aerobic sessions (six days per week). Cognitive function was assessed via a passive avoidance test in a shuttle box for learning and memory assessment. Hippocampal markers of oxidative stress and the expression of apoptosis-related genes (Bcl-2, Bax, and TGF-β) were quantified via biochemical assays and qPCR, respectively.

resultsCompared with saline, MA administration significantly impaired learning and memory, increasing the number of dark compartment entries (p < 0.0001). Aerobic training reversed these deficits by reducing entries and enhancing latency. Furthermore, MA increased hippocampal MDA levels and suppressed TAC (p < 0.0001), whereas exercise restored the oxidative balance. Gene expression analysis revealed MA-mediated upregulation of Bax and TGF-β, alongside decreased Bcl-2 (p < 0.0001), which were normalized by aerobic training.

conclusionThis study revealed that MIAT mitigated MA-induced cognitive deficits, oxidative stress, and apoptotic gene dysregulation in rats. Exercise normalized Bax, Bcl-2, and TGF-β expression; restored antioxidant levels and memory; and may be a clinically relevant, noninvasive intervention to support cognitive recovery in MA-exposed individuals.

Indexed as

Amphetamine-Related DisordersApoptosisBehavior, AnimalCentral Nervous System StimulantsHippocampusMethamphetaminePhysical Conditioning, AnimalAnimalsbcl-2-Associated X ProteinCognitionGene Expression RegulationMaleOxidative StressProto-Oncogene Proteins c-bcl-2RatsRats, Sprague-DawleyBax protein, ratbcl-2-Associated X ProteinBcl2 protein, ratCentral Nervous System StimulantsMethamphetamineProto-Oncogene Proteins c-bcl-2Transforming Growth Factor betaApoptosis markersBrain injuryExercise intensityGene expressionPassive avoidance test

Identifiers

PMID40643651

What Socratic holds

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Registered trials

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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 Socratic graph.