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Provedor de dados:  56
País:  Brazil
Título:  Activation of endogenous angiotensin converting enzyme 2 prevents early injuries induced by hyperglycemia in rat retina
Autores:  Foureaux,G.
Nogueira,B. S.
Coutinho,D. C. O.
Raizada,M. K.
Nogueira,J. C.
Ferreira,A. J.
Data:  2015-12-01
Ano:  2015
Palavras-chave:  ACE2 activation
Angiotensin-(1-7)
Renin-angiotensin system
Eyes
Diabetic retinopathy
Resumo:  Diabetic retinopathy (DR) is a serious complication of diabetes mellitus that may result in blindness. We evaluated the effects of activation of endogenous angiotensin converting enzyme (ACE) 2 on the early stages of DR. Rats were administered an intravenous injection of streptozotocin to induce hyperglycemia. The ACE2 activator 1-[[2-(dimethylamino) ethyl] amino]-4-(hydroxymethyl)-7-[[(4-methylphenyl) sulfonyl] oxy]-9H-xanthone 9 (XNT) was administered by daily gavage. The death of retinal ganglion cells (RGC) was evaluated in histological sections, and retinal ACE2, caspase-3, and vascular endothelial growth factor (VEGF) expressions were analyzed by immunohistochemistry. XNT treatment increased ACE2 expression in retinas of hyperglycemic (HG) rats (control: 13.81±2.71 area%; HG: 14.29±4.30 area%; HG+XNT: 26.87±1.86 area%; P<0.05). Importantly, ACE2 activation significantly increased the RCG number in comparison with HG animals (control: 553.5±14.29; HG: 530.8±10.3 cells; HG+XNT: 575.3±16.5 cells; P<0.05). This effect was accompanied by a reduction in the expression of caspase-3 in RGC of the HG+XNT group when compared with untreated HG rats (control: 18.74±1.59; HG: 38.39±3.39 area%; HG+XNT: 27.83±2.80 area%; P<0.05). Treatment with XNT did not alter the VEGF expression in HG animals (P>0.05). Altogether, these findings indicate that activation of ACE2 reduced the death of retinal ganglion cells by apoptosis in HG rats.
Tipo:  Info:eu-repo/semantics/article
Idioma:  Inglês
Identificador:  http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2015001201109
Editor:  Associação Brasileira de Divulgação Científica
Relação:  10.1590/1414-431x20154583
Formato:  text/html
Fonte:  Brazilian Journal of Medical and Biological Research v.48 n.12 2015
Direitos:  info:eu-repo/semantics/openAccess
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