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Provedor de dados:  BJMBR
País:  Brazil
Título:  Inflammation induced by increased frequency of intermittent hypoxia is attenuated by tempol administration
Autores:  Zhang,J.
Zheng,L.
Cao,J.
Chen,B.
Jin,D.
Data:  2015-12-01
Ano:  2015
Palavras-chave:  Obstructive sleep apnea
Intermittent hypoxia
Inflammation
Nuclear factor kappa B
Antioxidant
Resumo:  The levels of serum inflammatory cytokines and the activation of nuclear factor kappa B (NF-κB) and hypoxia inducible factor-1α (HIF-1α) in heart tissues in response to different frequencies of intermittent hypoxia (IH) and the antioxidant tempol were evaluated. Wistar rats (64 males, 200-220 g) were randomly divided into 6 experimental groups and 2 control groups. Four groups were exposed to IH 10, 20, 30, or 40 times/h. The other 2 experimental groups were challenged with IH (30 times/h) plus tempol, either beginning on day 0 (IH30T0) or on day 29 (IH30T29). After 6 weeks of challenge, serum levels of tumor necrosis factor (TNF)-α, intracellular adhesion molecule (ICAM)-1, and interleukin-10 were measured, and western blot analysis was used to detect NF-κB p65 and HIF-1α in myocardial tissues. Serum levels of TNF-α and ICAM-1 and myocardial expression of NF-κB p65 and HIF-1α were all significantly higher in IH rats than in controls (P<0.001). Increased IH frequency resulted in more significant changes. Administration of tempol in IH rats significantly reduced levels of TNF-α, ICAM-1, NF-κB and HIF-1α compared with the non-tempol-treated group (F=16.936, P<0.001). IH induced an inflammatory response in a frequency-dependent manner. Additionally, HIF-1α and NF-κB were increased following IH administration. Importantly, tempol treatment attenuated this effect.
Tipo:  Info:eu-repo/semantics/article
Idioma:  Inglês
Identificador:  http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2015001201115
Editor:  Associação Brasileira de Divulgação Científica
Relação:  10.1590/1414-431x20154487
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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