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首页> 外文期刊>American Journal of Physiology >Mitochondrial cytochrome c release is a key event in hyperoxia-induced lung injury: protection by cyclosporin A.
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Mitochondrial cytochrome c release is a key event in hyperoxia-induced lung injury: protection by cyclosporin A.

机译：线粒体细胞色素C释放是高氧诱导的肺损伤的关键事件：环孢菌素A的保护。

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摘要

Hyperoxia is known to induce extensive alveolar cell death by still poorly defined mechanisms. In this study, the mitochondria-dependent cell death pathway was explored during hyperoxia-induced lung injury in mice. We observed a progressive release of cytochrome c from the mitochondria into the cytosol of alveolar cells. This release was accompanied by the translocation of the proapoptotic protein Bax from cytosol to mitochondria without detectable activation of caspase-3. As cytochrome c release can be induced by mitochondrial membrane alteration and permeability transition (MPT), mice were treated with cyclosporin A, which specifically inhibits MPT. Cyclosporin A treatment prevented mitochondrial release of cytochrome c during hyperoxia and concomitantly preserved mitochondria from extensive swelling and crista disorganization, as assessed by electron microscopy analysis of alveolar epithelial cells. These morphological and biochemical observations correlated with decreased lung tissue damage, as evaluated by morphological score and lung weight. In conclusion, mitochondrial damage and cytochrome c release are important linked events in hyperoxia-induced lung injury and can be efficiently blocked by cyclosporin A.
机译：已知高氧通过仍不清楚的机制诱导广泛的肺泡细胞死亡。在这项研究中，在高氧诱导的小鼠肺损伤过程中探索了线粒体依赖性细胞死亡途径。我们观察到细胞色素c从线粒体逐渐释放到肺泡细胞的细胞质中。这种释放伴随着凋亡蛋白Bax从胞浆转移到线粒体，而没有检测到caspase-3的激活。由于线粒体膜改变和通透性转变（MPT）可以诱导细胞色素c的释放，因此用环孢菌素A治疗小鼠，后者特异性抑制MPT。环孢素A处理可防止高氧时线粒体释放细胞色素c，并同时防止线粒体因广泛的肿胀和cr状紊乱而保存，如通过肺泡上皮细胞的电子显微镜分析所评估的那样。这些形态和生化观察结果与肺组织损伤的减少相关，如通过形态学评分和肺重量评估。总之，线粒体损伤和细胞色素C释放是高氧引起的肺损伤中的重要关联事件，可以被环孢菌素A有效地阻断。

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