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

IF 3.9 4区医学 Q2 NEUROSCIENCES

NeuroMolecular Medicine Pub Date : 2025-07-26 DOI:10.1007/s12017-025-08876-8

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

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引用次数: 0

Abstract

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.

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探索参与缺血性中风和高压氧治疗潜力的核心基因：来自转录组学分析的见解。

缺血性中风（IS）是一种复杂的神经系统疾病，由脑血流量减少引起，通常由于缺氧和营养缺乏而导致组织损伤。高压氧治疗（HBOT）作为IS的辅助治疗显示出巨大的潜力，尽管其作用机制尚不完全清楚。本研究采用大脑中动脉闭塞（MCAO）小鼠模型，探讨HBOT的分子机制和治疗作用。转录组学分析显示，与缺血相关的基因表达发生了显著变化，包括参与炎症反应、血脑屏障损伤和神经修复的差异表达基因（deg），如Lcn2、Bcl3、Olr1、Pdpn、Gpnmb和Gfap。HBOT显著减少脑损伤，调节这些关键基因的表达，降低m6A甲基化水平，从而影响RNA的转录后修饰。这些发现为IS的分子机制和精确治疗策略的发展提供了新的见解，突出了HBOT在分子水平上减少脑损伤和促进神经修复的潜力。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

NeuroMolecular Medicine 医学-神经科学

CiteScore

7.10

自引率

0.00%

发文量

审稿时长

>12 weeks

期刊介绍： NeuroMolecular Medicine publishes cutting-edge original research articles and critical reviews on the molecular and biochemical basis of neurological disorders. Studies range from genetic analyses of human populations to animal and cell culture models of neurological disorders. Emerging findings concerning the identification of genetic aberrancies and their pathogenic mechanisms at the molecular and cellular levels will be included. Also covered are experimental analyses of molecular cascades involved in the development and adult plasticity of the nervous system, in neurological dysfunction, and in neuronal degeneration and repair. NeuroMolecular Medicine encompasses basic research in the fields of molecular genetics, signal transduction, plasticity, and cell death. The information published in NEMM will provide a window into the future of molecular medicine for the nervous system.