title: Angiotensin-(1-7) relieved renal injury induced by chronic intermittent hypoxia in rats by reducing inflammation, oxidative stress and fibrosis.
abstract: 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.
authors.affiliation: Division of Respiratory Disease, Renmin Hospital of Wuhan University, Wuhan, China.
authors.forename: W
authors.initials: W
authors.lastname: Lu
authors.affiliation: Division of Respiratory Disease, Renmin Hospital of Wuhan University, Wuhan, China.
authors.forename: J
authors.initials: J
authors.lastname: Kang
authors.affiliation: Division of Respiratory Disease, Renmin Hospital of Wuhan University, Wuhan, China.
authors.forename: K
authors.initials: K
authors.lastname: Hu
authors.affiliation: Division of Respiratory Disease, Renmin Hospital of Wuhan University, Wuhan, China.
authors.forename: S
authors.initials: S
authors.lastname: Tang
authors.affiliation: Division of Respiratory Disease, Renmin Hospital of Wuhan University, Wuhan, China.
authors.forename: X
authors.initials: X
authors.lastname: Zhou
authors.affiliation: Division of Respiratory Disease, Renmin Hospital of Wuhan University, Wuhan, China.
authors.forename: S
authors.initials: S
authors.lastname: Yu
authors.affiliation: Division of Respiratory Disease, Renmin Hospital of Wuhan University, Wuhan, China.
authors.forename: L
authors.initials: L
authors.lastname: Xu
mesh_terms: D058186:Acute Kidney Injury / Q000188:drug therapy*; D000803:Angiotensin I / Q000008:administration & dosage*; D000818:Animals; D004195:Disease Models, Animal; D007249:Inflammation / Q000188:drug therapy; D015850:Interleukin-6 / Q000378:metabolism; D007668:Kidney / Q000378:metabolism / Q000473:pathology; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects*; D010446:Peptide Fragments / Q000008:administration & dosage*; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: C508600:IL6 protein, human; D015850:Interleukin-6; D010446:Peptide Fragments; D000803:Angiotensin I; C118790:angiotensin I (1-7)