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<p>Ischemia-reperfusion (I/R) injury critically impairs neuronal survival, with mitochondrial dysfunction being a&#xa0;central pathogenic factor. Although mild hypothermia has demonstrated neuroprotective potential, the precise mechanisms involving mitochondrial regulation remain incompletely understood. This study investigates whether mild hypothermia protects neurons by preserving mitochondrial membrane potential (MMP) and modulating key mitochondrial apoptosis-related proteins, including caspase‑3, Cytochrome&#xa0;c (Cyt&#xa0;c), Bax, and Bcl‑2. In an <i>in vivo I/R model</i>, nasopharyngeal cavity cooling significantly enhanced neuronal MMP and altered the expression of mitochondrial injury-related proteins. These findings were corroborated in an <i>in vitro oxygen-glucose deprivation/reoxygenation (OGD/R) model</i>, where mild hypothermia also improved MMP and reduced neuronal damage and death. Concurrently, our results indicate that mild hypothermia mitigates neuronal injury by restoring MMP and suppressing the mitochondrial apoptotic pathway. These insights not only elucidate a&#xa0;mechanistic basis for mild hypothermia-induced neuroprotection but also reinforce the therapeutic relevance of mitochondria in I/R injury, supporting the clinical translation of nasopharyngeal cavity cooling for brain protection.</p>

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Effects of mild hypothermia on neuronal mitochondrial membrane potential and apoptosis in vivo and in vitro

  • 期刊论文

  • 发表日期：

    2025年12月1日

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  • Zheng Liu,
  • Xiaorui Xi,
  • Dongyang Ma,
  • Zan Gao,
  • Shan Zhang,
  • Zhiqiang Zhang

摘要

Ischemia-reperfusion (I/R) injury critically impairs neuronal survival, with mitochondrial dysfunction being a central pathogenic factor. Although mild hypothermia has demonstrated neuroprotective potential, the precise mechanisms involving mitochondrial regulation remain incompletely understood. This study investigates whether mild hypothermia protects neurons by preserving mitochondrial membrane potential (MMP) and modulating key mitochondrial apoptosis-related proteins, including caspase‑3, Cytochrome c (Cyt c), Bax, and Bcl‑2. In an in vivo I/R model, nasopharyngeal cavity cooling significantly enhanced neuronal MMP and altered the expression of mitochondrial injury-related proteins. These findings were corroborated in an in vitro oxygen-glucose deprivation/reoxygenation (OGD/R) model, where mild hypothermia also improved MMP and reduced neuronal damage and death. Concurrently, our results indicate that mild hypothermia mitigates neuronal injury by restoring MMP and suppressing the mitochondrial apoptotic pathway. These insights not only elucidate a mechanistic basis for mild hypothermia-induced neuroprotection but also reinforce the therapeutic relevance of mitochondria in I/R injury, supporting the clinical translation of nasopharyngeal cavity cooling for brain protection.