Exogenous surfactant prevents hyperoxiainduced lung injury in adult mice.

• Autor(a) principal: Bezerra, Frank Silva
• Data de Publicação: 2019
• Outros Autores: Ramos, Camila de Oliveira, Castro, Thalles de Freitas, Araújo, Natália Pereira da Silva, Souza, Ana Beatriz Farias de, Bandeira, Ana Carla Balthar, Costa, Guilherme de Paula, Cartelle, Christiane Teixeira, Silva, André Talvani Pedrosa da, Cangussú, Silvia Dantas, Brochard, Laurent Jean, Nagato, Akinori Cardozo
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Repositório Institucional da UFOP
• Texto Completo: http://www.repositorio.ufop.br/handle/123456789/11979; https://doi.org/10.1186/s40635-019-0233-6
• topic: BALB/c mice; Oxidative stress

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 surfactante 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 antioxidante 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.