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<p>Exercise training can exert favorable effects on the remodeling of neural structures, functional reconstruction, and the recovery of neurovascular units after cerebral ischemia. It has also been documented to activate the JNK/c-jun pathway, which is involved in diverse cellular processes, including growth regulation, transformation, and programmed cell death. However, it remains obscure regarding the role of the JNK/c-jun pathway in the aforementioned exercise training–conferred neurological benefits. In this study, rats received exercise training after transient middle cerebral artery occlusion. The potential impact of exercise training on apoptosis, nerve remodeling, functional remodeling, and vascular regeneration was investigated by Western blotting, immunofluorescence staining, transmission electron microscopy, Golgi staining, Tunel staining, and neurological function assessment, etc. Exercise training activated the JNK/c-jun pathway, which was closely linked with cerebral ischemia–reperfusion (I/R) injury. The training mitigated cerebral I/R injury-induced cell apoptosis and promoted neural structural remodeling, neurological function recovery, and vascular regeneration in the ischemic penumbra. However, the protective benefits of exercise training were offset by the JNK inhibitor, SP600125. After cerebral ischemia, exercise training can promote neural structural remodeling, neurological functional recovery, and vascular regeneration. These processes may be achieved by activating the JNK/c-jun signaling pathway.</p>

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Exercise Training Promotes Neural Remodeling and Vascular Regeneration in Cerebral Ischemic Rats Through the JNK/c-jun Signaling Pathway

  • 期刊论文

  • 发表日期：

    2025年6月7日

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  • Zijun Zhao,
  • Xiuyun Chen,
  • Zezhong Zhuang,
  • Jianmin Chen,
  • Zhijian Zheng,
  • Wenwen Wu,
  • Zhiyun Wu,
  • Qiang Lin,
  • Manli Chen,
  • Ji Liu,
  • Nan Liu,
  • Ronghua Chen,
  • Hongbin Chen

摘要

Exercise training can exert favorable effects on the remodeling of neural structures, functional reconstruction, and the recovery of neurovascular units after cerebral ischemia. It has also been documented to activate the JNK/c-jun pathway, which is involved in diverse cellular processes, including growth regulation, transformation, and programmed cell death. However, it remains obscure regarding the role of the JNK/c-jun pathway in the aforementioned exercise training–conferred neurological benefits. In this study, rats received exercise training after transient middle cerebral artery occlusion. The potential impact of exercise training on apoptosis, nerve remodeling, functional remodeling, and vascular regeneration was investigated by Western blotting, immunofluorescence staining, transmission electron microscopy, Golgi staining, Tunel staining, and neurological function assessment, etc. Exercise training activated the JNK/c-jun pathway, which was closely linked with cerebral ischemia–reperfusion (I/R) injury. The training mitigated cerebral I/R injury-induced cell apoptosis and promoted neural structural remodeling, neurological function recovery, and vascular regeneration in the ischemic penumbra. However, the protective benefits of exercise training were offset by the JNK inhibitor, SP600125. After cerebral ischemia, exercise training can promote neural structural remodeling, neurological functional recovery, and vascular regeneration. These processes may be achieved by activating the JNK/c-jun signaling pathway.