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慢性间歇性缺氧诱导的隔膜肌肉衰弱是依赖NADPH氧化酶-2的
Sarah E Drummond1, David P Burns1, Sarah El Maghrani1
1Department of Physiology, School of Medicine, College of Medicine and Health, University College Cork, T12 XF62 Cork, Ireland.
NADPH氧化酶2 (NOX2) 有助于由慢性间歇性缺氧 (CIH) 引起的隔膜肌肉功能障碍. 阻断NOX2可以防止这种弱点,这表明NOX2抑制是CIH相关呼吸系统问题的潜在治疗方法.
科学领域:
- 生理学 生理学 生理学
- 分子生物学分子生物学
- 呼吸系统医学 呼吸系统医学
背景情况:
- 慢性间歇性缺氧 (CIH) 通过氧化还原变化导致隔膜肌肉功能障碍.
- 在CIH引起的隔膜功能障碍中NADPH氧化酶2 (NOX2) 的特定作用尚不清楚.
研究的目的:
- 调查NOX2衍生反应性氧物种 (ROS) 是否介导CIH诱导的隔膜肌功能障碍.
- 评估NOX2抑制在预防CIH诱导的隔膜软弱方面的治疗潜力.
主要方法:
- 成年雄性小鼠被暴露于CIH14天.
- 小鼠接受了NOX2抑制剂 (apocynin) 或在NOX2 (NOX2-null) 中遗传缺乏.
- 分析了隔膜肌肉性能和基因表达.
主要成果:
- 阿波基尼治疗和NOX2删除完全防止了CIH诱导的腹膜肌功能障碍.
- CIH暴露增加了NOX4mRNA,但没有增加NOX2的表达.
- 观察到参与肌肉再生,抗氧化能力,自和缩的基因的NOX2依赖上调.
结论:
- NOX2衍生的ROS在CIH诱导的腹膜肌功能障碍中发挥着关键作用.
- NOX2阻塞是一种有前途的治疗策略,用于改善阻塞性睡眠呼吸暂停等条件下的隔膜性能.
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