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Hypercapnic acidosis attenuates pulmonary epithelial stretch-induced injury via inhibition of the canonical NF-κB pathway

机译:高碳酸血症性酸中毒通过抑制经典的NF-κB途径减轻肺上皮牵张引起的损伤

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摘要

BackgroundHypercapnia, with its associated acidosis (HCA), is a consequence of respiratory failure and is also seen in critically ill patients managed with conventional “protective” ventilation strategies. Nuclear factor kappa-B (NF-κB), a pivotal transcription factor, is activated in the setting of injury and repair and is central to innate immunity. We have previously established that HCA protects against ventilation-induced lung injury in vivo, potentially via a mechanism involving inhibition of NF-κB signaling. We wished to further elucidate the role and mechanism of HCA-mediated inhibition of the NF-κB pathway in attenuating stretch-induced injury in vitro.
机译:背景高碳酸血症及其相关的酸中毒(HCA)是呼吸衰竭的结果,在采用常规“保护性”通气策略治疗的重症患者中也可见到。关键转录因子核因子κB(NF-κB)在损伤和修复过程中被激活,是先天免疫的关键。我们先前已经确定,HCA可能通过涉及抑制NF-κB信号传导的机制,在体内预防通气诱发的肺损伤。我们希望进一步阐明HCA介导的NF-κB通路抑制作用在体外减轻拉伸引起的损伤中的作用和机制。

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