Data/hora: 11/06/2024 06:48:14

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&lt;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&lt;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&lt;0.05). Treatment with XNT did not alter the VEGF expression in HG animals (P&gt;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	
Fonte: 	info:eu-repo/semantics/openAccess