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Purpose <p>Stroke is one of the debilitating diseases that can lead to organ paralysis and reduced productivity. As a non-pharmalogical approach to treatment, endurance training can improve the symptoms of disability and induce repair of damaged tissues. Apoptosis of sensory-motor neurons is one of the most important mechanisms of nerve damage in stroke, and its inhibition in the early hours after ischemia would be very effective in reducing the complications of the disease. We aimed to evaluate if early exercise training following common carotid artery (CCA) ischemia can modulate apoptosis-related markers, influence neuronal survival in the CA1 region of the hippocampus, and improve motor function recovery.</p> Methods <p>Thirty-six Wistar male rats were divided in three groups (<i>n</i> = 12); control, CCA ischemia, and CCA ischemia + exercise. The ischemic model was created by a 45-min occlusion of the CCA. The Ladder rung test was executed in 2&#xa0;h, 24&#xa0;h, 1&#xa0;week and 8&#xa0;weeks after ischemia induction to assess motor function capacity. The <i>Bax</i> and <i>BCL2</i> gene and protein expression levels were quantified with quantitative PCR and histological tissue staining, respectively.</p> Results <p>Compared to control, the Bax expression was higher in ischemic rats and was decreased in the exercise group. The Bcl2 expression was lower in ischemic rats and increased after exercise. The walking ability improved after exercise and the dead cells percentage was lower than in no-intervention ischemic group.</p> Conclusion <p>Endurance training can reduce the levels of apoptotic factors and improve the motor ability of ischemic rats after 8&#xa0;weeks of exercise. Thus, it would be an important approach for improving the motor’s postoperative complication.</p>

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Post-Conditioning Endurance Training Effect on Apoptosis Inhibition of Hippocampus Neurons in Common Carotid Artery Ischemia Models

  • 期刊论文

  • 发表日期：

    2026年2月5日

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  • Ali Golestani,
  • Zahra Eslami,
  • Shima Gholamalipor,
  • Malihe Milani,
  • Seyed Javad Mirghani

摘要

Purpose

Stroke is one of the debilitating diseases that can lead to organ paralysis and reduced productivity. As a non-pharmalogical approach to treatment, endurance training can improve the symptoms of disability and induce repair of damaged tissues. Apoptosis of sensory-motor neurons is one of the most important mechanisms of nerve damage in stroke, and its inhibition in the early hours after ischemia would be very effective in reducing the complications of the disease. We aimed to evaluate if early exercise training following common carotid artery (CCA) ischemia can modulate apoptosis-related markers, influence neuronal survival in the CA1 region of the hippocampus, and improve motor function recovery.

Methods

Thirty-six Wistar male rats were divided in three groups (n = 12); control, CCA ischemia, and CCA ischemia + exercise. The ischemic model was created by a 45-min occlusion of the CCA. The Ladder rung test was executed in 2 h, 24 h, 1 week and 8 weeks after ischemia induction to assess motor function capacity. The Bax and BCL2 gene and protein expression levels were quantified with quantitative PCR and histological tissue staining, respectively.

Results

Compared to control, the Bax expression was higher in ischemic rats and was decreased in the exercise group. The Bcl2 expression was lower in ischemic rats and increased after exercise. The walking ability improved after exercise and the dead cells percentage was lower than in no-intervention ischemic group.

Conclusion

Endurance training can reduce the levels of apoptotic factors and improve the motor ability of ischemic rats after 8 weeks of exercise. Thus, it would be an important approach for improving the motor’s postoperative complication.