Data/hora: 08/06/2024 03:48:41

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