首页> 外文期刊>Anesthesiology >Heme Oxygenase-1/Carbon Monoxide-regulated Mitochondrial Dynamic Equilibrium Contributes to the Attenuation of Endotoxin-induced Acute Lung Injury in Rats and in Lipopolysaccharide-activated Macrophages
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Heme Oxygenase-1/Carbon Monoxide-regulated Mitochondrial Dynamic Equilibrium Contributes to the Attenuation of Endotoxin-induced Acute Lung Injury in Rats and in Lipopolysaccharide-activated Macrophages

机译:血红素加氧酶-1 /一氧化碳调节的线粒体动态平衡有助于减轻内毒素诱导的大鼠和脂多糖激活的巨噬细胞的急性肺损伤。

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Background: Sepsis-associated acute lung injury remains the major cause of mortality in critically ill patients and is characterized by marked oxidative stress and mitochondrial dysfunction. Mitochondrial dynamics are indispensable for functional integrity. Additionally, heme oxygenase (HO)-1/carbon monoxide conferred cytoprotection against end-organ damage during endotoxic shock. Herein, we tested the hypothesis that HO-1/carbon monoxide played a critical role in maintaining the dynamic process of mitochondrial fusion/fission to mitigate lung injury in Sprague-Dawley rats or RAW 264.7 macrophages exposed to endotoxin.
机译:背景:脓毒症相关的急性肺损伤仍然是重症患者死亡的主要原因,其特征是氧化应激和线粒体功能异常。线粒体动力学对于功能完整性是必不可少的。此外,血红素加氧酶(HO)-1 /一氧化碳赋予了细胞内毒素休克期间抵抗终末器官损害的细胞保护作用。本文中,我们测试了以下假设:HO-1 /一氧化碳在维持线粒体融合/裂变的动态过程以减轻Sprague-Dawley大鼠或暴露于内毒素的RAW 264.7巨噬细胞的肺损伤中起着关键作用。

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