首页> 外文会议>Bioengineering Conference (NEBEC), 2012 38th Annual Northeast >Cyclic stretch induced oxidative injury increases alveolar permeability via ERK-NF-κB signaling
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Cyclic stretch induced oxidative injury increases alveolar permeability via ERK-NF-κB signaling

机译:循环拉伸诱导的氧化损伤通过ERK-NF-κB信号传导增加肺泡通透性

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The mechanisms underlying cyclic-stretch induced increase in pulmonary alveolar epithelial permeability are not yet fully elucidated. Here we demonstrate high levels of superoxide and nitric oxide in type I alveolar epithelial cells that were stretched at 12 and 37% change in surface area for different time durations. Cyclic stretch induced increase in permeability was decreased by the supeoxide scavenger Tiron and by the NF-κB inhibitor MG132. Furthermore, cyclic stretch increased the activation of the NF-κB signaling pathway which was significantly decreased with ERK inhibitor U0126. These data suggest that cyclic stretch induces oxidative stress, which mediates increases in alveolar epithelial monolayer permeability via NF-κB activation and ERK phosphorylation.
机译:循环拉伸诱导的肺泡上皮通透性增加的机制尚未完全阐明。在这里,我们证明了I型肺泡上皮细胞中高水平的超氧化物和一氧化氮,它们在不同的持续时间内表面积分别以12%和37%的变化拉伸。超氧化物清除剂Tiron和NF-κB抑制剂MG132降低了循环拉伸诱导的通透性增加。此外,循环拉伸增加了NF-κB信号通路的激活,而ERK抑制剂U0126则明显降低了激活。这些数据表明循环拉伸诱导氧化应激,其通过NF-κB活化和ERK磷酸化介导肺泡上皮单层渗透性的增加。

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