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Provedor de dados:  Anais da ABC (AABC)
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
Direitos:  info:eu-repo/semantics/openAccess
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