| Registro completo |
| Provedor de dados: |
BJMBR
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| País: |
Brazil
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| Título: |
Angiotensin-(1–7) inhibits inflammation and oxidative stress to relieve lung injury induced by chronic intermittent hypoxia in rats
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| Autores: |
Lu,W.
Kang,J.
Hu,K.
Tang,S.
Zhou,X.
Yu,S.
Li,Y.
Xu,L.
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| Data: |
2016-01-01
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| Ano: |
2016
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| Palavras-chave: |
Ang-(1–7)
Lung injury
Obstructive sleep apnea
Inflammation
Oxidative stress
Chronic intermittent hypoxia
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| 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<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.
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| Tipo: |
Info:eu-repo/semantics/article
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| Idioma: |
Inglês
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| Identificador: |
http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2016001000603
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| Editor: |
Associação Brasileira de Divulgação Científica
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| Relação: |
10.1590/1414-431x20165431
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| Formato: |
text/html
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| Fonte: |
Brazilian Journal of Medical and Biological Research v.49 n.10 2016
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| Direitos: |
info:eu-repo/semantics/openAccess
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