高压氧增加了线粒体生物发生和功能与氧化应激在HL-1心肌细胞中的氧化应激
Ha-Yeong Young1,2, Sunchul Lee1,2, Yeo-Eun Choi3
1Department of Physiology and Global Medical Science, Yonsei University Wonju College of Medicine, Wonju, Republic of Korea.
Journal of applied physiology (Bethesda, Md. : 1985)
|May 22, 2025
概括
高压氧气疗法通过氧化应激增强心脏细胞线粒体功能和抗氧化防御. 然而,它可能会损害具有先前存在的线粒体缺陷的细胞,表明双重效应.
科学领域:
- 线粒体生理学线粒体生理学
- 细胞应激反应 细胞应激反应
- 高压医学的高压医学.
背景情况:
- 高压氧气 (HBO2) 疗法用于CO中毒和缺血-再输液损伤等疾病.
- 在HBO2的治疗效益背后的精确分子机制尚未完全理解.
- 研究HBO2对细胞线粒体的影响对于理解其影响至关重要.
研究的目的:
- 阐明高压氧 (HBO2) 治疗对线粒体功能和生物发生的分子机制.
- 检查心肌细胞中HBO2诱导的活性氧物种 (ROS),基因表达和线粒体参数的变化.
- 评估HBO2暴露对心肌细胞跳动活动的功能影响.
主要方法:
- 在受控条件下,HL-1心肌细胞被暴露在高压氧 (HBO2) 中.
- 测量包括活性氧物种 (ROS),基因转录/翻译,线粒体膜潜力 (ΔΨm),呼吸,ATP含量和细胞跳动.
- 研究涉及有或没有线粒体电子运输链抑制剂预处理的细胞.
主要成果:
- 暴露于HBO2会增加细胞质和线粒体ROS的产生,从而提高压力反应基因的调节 (GDF15,FGF21).
- HBO2增强了抗氧化剂信号传递 (Nrf2) 和线粒体生物发生 (PGC-1α),改善了线粒体的氧气消耗, ΔΨm 和 ATP 生产.
- HBO2增加了心肌细胞跳动集群,但在具有先前存在缺陷的细胞中加剧了线粒体功能障碍.
结论:
- HBO2诱导的氧化应激触发了保护性反应,增强了线粒体生物发生和心肌细胞中的功能.
- 通过压力反应途径和改善线粒体健康,HBO2的有益作用是介导的.
- HBO2可能对线粒体功能受损的细胞有害,强调需要仔细的治疗考虑.
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