Data/hora: 03/06/2024 18:18:26

Provedor de dados: 	42	
País: 	Brazil	
Título: 	Candesartan inhibits inflammation through an angiotensin II type 1 receptor independent way in human embryonic kidney epithelial cells	
Autores: 	YU,YING; JIANG,HAIFENG; NIU,YANGYANG; ZHANG,XIAOQIN; ZHANG,YINGYING; LIU,XI; QI,TAO; YU,CHEN.	
Data: 	2019-01-01	
Ano: 	2019	
Palavras-chave: 	Angiotensin II type 1 receptor blockers; Candesartan; Inflammation; Reactive oxygen species.	
Resumo: 	Abstract: Besides stimulating vasoconstriction, Angiotensin II is also well known in inducing reactive oxygen species and promoting inflammatory phenotype switch via its type 1 receptor. In clinic, Angiotensin II type 1 (AT1) receptor blocker like candesartan has been widely applied as an antihypertensive medication. We previous have demonstrated that a higher dose of candesartan plays a protective role after kidney injury. However, whether candesartan could exhibit anti-inflammatory effects remains unclear. Here, by stimulating isolated human embryonic kidney epithelial cells with tumor necrosis factor-α (TNF-α), we observed the anti-inflammation capacity of candesartan ex vivo. It was found that pre-treat with candesartan significantly suppressed transforming growth factor-β (TGF-β) and interleukin-6 (IL-6) expression after incubation with TNF-α. Surprisingly, silence of angiotensin II type 1 receptor has little effects on reducing TGF-β or IL-6 products. Furthermore, candesartan inhibited TNF-α-induced oxidative stress in the primary cultured tubular epithelial cells. Overall, our data indicates that candesartan suppresses TNF-α-induced inflammatory cytokine production by inhibiting oxidative stress, rather than block AT1 receptor activity.	
Tipo: 	Info:eu-repo/semantics/article	
Idioma: 	Inglês	
Identificador: 	http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0001-37652019000300701	
Editor: 	Academia Brasileira de Ciências	
Relação: 	10.1590/0001-3765201920180699	
Formato: 	text/html	
Fonte: 	Anais da Academia Brasileira de Ciências  v.91 n.2 2019	
Fonte: 	info:eu-repo/semantics/openAccess