Data/hora: 09/06/2024 06:15:31

Provedor de dados: 	56	
País: 	Brazil	
Título: 	Angiotensin-(1-7) relieved renal injury induced by chronic intermittent hypoxia in rats by reducing inflammation, oxidative stress and fibrosis	
Autores: 	Lu,W.; Kang,J.; Hu,K.; Tang,S.; Zhou,X.; Yu,S.; Xu,L.	
Data: 	2017-01-01	
Ano: 	2017	
Palavras-chave: 	Ang(1-7); Renal injury; Obstructive sleep apnea; Inflammation; Oxidative stress; Fibrosis.	
Resumo: 	We aimed to study the renal injury and hypertension induced by chronic intermittent hypoxia (CIH) and the protective effects mediated by angiotensin 1-7 [Ang(1-7)]. We randomly assigned 32 male Sprague-Dawley rats (body weight 180-200 g) to normoxia control, CIH, Ang(1-7)-treated normoxia, and Ang(1-7)-treated CIH groups. Systolic blood pressure (SBP) was monitored at the start and end of each week. Renal sympathetic nerve activity (RSNA) was recorded. CTGF and TGF-β were detected by immunohistochemistry and western blotting. Tissue parameters of oxidative stress were also determined. In addition, renal levels of interleukin-6, tumor necrosis factor-α, nitrotyrosine, and hypoxia-inducible factor-1α were determined by immunohistochemistry, immunoblotting, and ELISA. TUNEL assay results and cleaved caspase 3 and 12 were also determined. Ang(1-7) induced a reduction in SBP together with a restoration of RSNA in the rat model of CIH. Ang(1-7) treatment also suppressed the production of reactive oxygen species, reduced renal tissue inflammation, ameliorated mesangial expansion, and decreased renal fibrosis. Thus, Ang(1-7) treatment exerted renoprotective effects on CIH-induced renal injury and was associated with a reduction of oxidative stress, inflammation and fibrosis. Ang(1-7) might therefore represent a promising therapy for obstructive sleep apnea-related hypertension and renal injury.	
Tipo: 	Info:eu-repo/semantics/article	
Idioma: 	Inglês	
Identificador: 	http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2017000100604	
Editor: 	Associação Brasileira de Divulgação Científica	
Relação: 	10.1590/1414-431x20165594	
Formato: 	text/html	
Fonte: 	Brazilian Journal of Medical and Biological Research  v.50 n.1 2017	
Fonte: 	info:eu-repo/semantics/openAccess