Data/hora: 13/05/2024 18:26:54

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