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Purpose <p>Methamphetamine (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.</p> Methods <p>Forty male rats were randomly assigned to four groups (Saline, MA, MA + MIAT, and MIAT) and given increasing MA doses (2.5–10&#xa0;mg/kg) over 23&#xa0;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 (<i>Bcl-2</i>, <i>Bax</i>, and <i>TGF-β</i>) were quantified via biochemical assays and qPCR, respectively.</p> Results <p>Compared with saline, MA administration significantly impaired learning and memory, increasing the number of dark compartment entries (p &lt; 0.0001). Aerobic training reversed these deficits by reducing entries and enhancing latency. Furthermore, MA increased hippocampal MDA levels and suppressed TAC (p &lt; 0.0001), whereas exercise restored the oxidative balance. Gene expression analysis revealed MA-mediated upregulation of <i>Bax</i> and <i>TGF-β</i>, alongside decreased <i>Bcl-2</i> (p &lt; 0.0001), which were normalized by aerobic training.</p> Conclusion <p>This study revealed that MIAT mitigated MA-induced cognitive deficits, oxidative stress, and apoptotic gene dysregulation in rats. Exercise normalized <i>Bax</i>, <i>Bcl-2</i>, and <i>TGF-β</i> expression; restored antioxidant levels and memory; and may be a clinically relevant, noninvasive intervention to support cognitive recovery in MA-exposed individuals.</p>

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

  • 期刊论文

  • 发表日期：

    2025年7月11日

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

摘要

Purpose

Methamphetamine (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.

Methods

Forty 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.

Results

Compared 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.

Conclusion

This 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.