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<p>Ischemic stroke (IS) is a complex neurological disorder caused by reduced cerebral blood flow, typically resulting in tissue damage due to hypoxia and nutrient deficiency. Hyperbaric oxygen therapy (HBOT) has shown great potential as an adjunctive treatment for IS, though its mechanisms of action are not fully understood. This study employed a middle cerebral artery occlusion (MCAO) mouse model to explore the molecular mechanisms and therapeutic effects of HBOT. Transcriptomic analysis revealed significant changes in gene expression related to ischemia, including differentially expressed genes (DEGs) involved in inflammatory responses, BBB damage, and neural repair, such as <i>Lcn2</i>, <i>Bcl3</i>, <i>Olr1</i>, <i>Pdpn</i>, <i>Gpnmb</i>, and <i>Gfap</i>. HBOT significantly reduced brain damage, modulated the expression of these key genes, and decreased m<sup>6</sup>A methylation levels, thereby affecting post-transcriptional modifications of RNA. These findings provide new insights into the molecular mechanisms of IS and the development of precise treatment strategies, highlighting the potential of HBOT to reduce brain damage and promote neural repair at the molecular level.</p>

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Exploring Core Genes Involved in Ischemic Stroke and the Therapeutic Potential of Hyperbaric Oxygen: Insights from Transcriptomic Analysis

  • 期刊论文

  • 发表日期：

    2025年7月26日

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  • Yingcun Bao,
  • Xudong Guo,
  • Jinhai Wang,
  • Jihe Kang,
  • Rui Ma,
  • Xiaorong Cheng,
  • Yumei Ma,
  • Yanxia Niu,
  • Wei Zhang,
  • Xiaoling Li

摘要

Ischemic stroke (IS) is a complex neurological disorder caused by reduced cerebral blood flow, typically resulting in tissue damage due to hypoxia and nutrient deficiency. Hyperbaric oxygen therapy (HBOT) has shown great potential as an adjunctive treatment for IS, though its mechanisms of action are not fully understood. This study employed a middle cerebral artery occlusion (MCAO) mouse model to explore the molecular mechanisms and therapeutic effects of HBOT. Transcriptomic analysis revealed significant changes in gene expression related to ischemia, including differentially expressed genes (DEGs) involved in inflammatory responses, BBB damage, and neural repair, such as Lcn2, Bcl3, Olr1, Pdpn, Gpnmb, and Gfap. HBOT significantly reduced brain damage, modulated the expression of these key genes, and decreased m6A methylation levels, thereby affecting post-transcriptional modifications of RNA. These findings provide new insights into the molecular mechanisms of IS and the development of precise treatment strategies, highlighting the potential of HBOT to reduce brain damage and promote neural repair at the molecular level.