Exogenous surfactant prevents hyperoxia-induced lung injury in adult mice
Exogenous surfactant prevents hyperoxia-induced lung injury in adult mice
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DOI：
10.1186/s40635-019-0233-6
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发表时间：
2019-03-27
影响因子：
3.5
通讯作者：
Nagato, Akinori Cardozo
中科院分区：
文献类型：
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作者：
Bezerra, Frank Silva;Ramos, Camila de Oliveira;Nagato, Akinori Cardozo
背景资料：除了发生呼吸机诱导的肺损伤的风险外，ARDS患者还存在发生高氧损伤的风险，这是由于临床上需要超生理氧气补充来逆转低氧血症。内源性表面活性物质系统的改变参与了急性呼吸窘迫综合征（ARDS）时肺功能障碍的发生。外源性肺表面活性物质对高氧损伤有保护作用（8-10周），一种对高氧高度敏感的品系，在吸入室中暴露于高氧24小时之前12小时通过鼻内滴注接受外源性含表面活性剂的蛋白SP-B和SP-C，并与仅接受高氧的小鼠和接受常氧的对照小鼠进行比较。与高氧组相比，外源性表面活性剂的给药能够通过减少中性粒细胞和炎症生物标志物（如TNF、IL-17和HMGB 1表达）的流入来减轻肺部炎症。抗氧化活性通过减少脂质过氧化和蛋白质羰基化，增加超氧化物歧化酶活性，防止氧化损伤时相比，高氧group.Conclusion：我们的研究结果提供了新的观点外源性表面活性物质在保护气道和肺，在富氧肺微环境中，对氧化损伤和急性炎症加重高氧诱导的影响和机制。
Background: In addition to the risk of developing ventilator-induced lung injury, patients with ARDS are at risk of developing hyperoxic injury due the supra-physiological oxygen supplementation clinically required to reverse hypoxemia. Alterations of endogenous surfactant system participate in the pulmonary dysfunction observed in ARDS. Administration of exogenous surfactant could have protective effects during hyperoxia.Methods: Male BALB/c mice (8-10 weeks), a strain highly sensitive to hyperoxia, received the exogenous surfactant-containing protein SP-B and SP-C by intranasal instillation 12 h before starting 24 h of exposure to hyperoxia in an inhalation chamber and were compared to mice receiving hyperoxia alone and to controls subjected to normoxia.Results: Compared to the hyperoxia group, the administration of exogenous surfactant was able to reduce lung inflammation through a reduction in the influx of neutrophils and inflammatory biomarkers such as TNF, IL-17, and HMGB1 expression. The antioxidant activity prevented oxidative damage by reducing lipid peroxidation and protein carbonylation and increasing superoxide dismutase activity when compared to the hyperoxia group.Conclusion: Our results offer new perspectives on the effects and the mechanism of exogenous surfactant in protecting the airway and lungs, in oxygen-rich lung microenvironment, against oxidative damage and aggravation of acute inflammation induced by hyperoxia.