Data/hora: 14/05/2024 09:29:20

Provedor de dados: | 56
País: | Brazil
Título: | Angiotensin-(1–7) inhibits inflammation and oxidative stress to relieve lung injury induced by chronic intermittent hypoxia in rats
Autores: | Lu,W.; Kang,J.; Hu,K.; Tang,S.; Zhou,X.; Yu,S.; Li,Y.; Xu,L.
Data: | 2016-01-01
Ano: | 2016
Palavras-chave: | Ang-(1–7); Lung injury; Obstructive sleep apnea; Inflammation; Oxidative stress; Chronic intermittent hypoxia.
Resumo: | Obstructive sleep apnea is associated with inflammation and oxidative stress in lung tissues and can lead to metabolic abnormalities. We investigated the effects of angiotensin1–7 [Ang-(1–7)] on lung injury in rats induced by chronic intermittent hypoxia (CIH). We randomly assigned 32 male Sprague-Dawley rats (180–200 g) to normoxia control (NC), CIH-untreated (uCIH), Ang-(1–7)-treated normoxia control (N-A), and Ang-(1–7)-treated CIH (CIH-A) groups. Oxidative stress biomarkers were measured in lung tissues, and expression of NADPH oxidase 4 (Nox4) and Nox subunits (p22phox, and p47phox) was determined by Western blot and reverse transcription-polymerase chain reaction. Pulmonary pathological changes were more evident in the uCIH group than in the other groups. Enzyme-linked immunosorbent assays and immunohistochemical staining showed that inflammatory factor concentrations in serum and lung tissues in the uCIH group were significantly higher than those in the NC and N-A groups. Expression of inflammatory factors was significantly higher in the CIH-A group than in the NC and N-A groups, but was lower than in the uCIH group (P&lt;0.01). Oxidative stress was markedly higher in the uCIH group than in the NC and N-A groups. Expression of Nox4 and its subunits was also increased in the uCIH group. These changes were attenuated upon Ang-(1–7) treatment. In summary, treatment with Ang-(1-7) reversed signs of CIH-induced lung injury via inhibition of inflammation and oxidative stress.
Tipo: | Info:eu-repo/semantics/article
Idioma: | Inglês
Identificador: | http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2016001000603
Editor: | Associação Brasileira de Divulgação Científica
Relação: | 10.1590/1414-431x20165431
Formato: | text/html
Fonte: | Brazilian Journal of Medical and Biological Research  v.49 n.10 2016
Fonte: | info:eu-repo/semantics/openAccess