دورية أكاديمية

Propofol pretreatment attenuates lipopolysaccharide-induced acute lung injury in rats by activating the phosphoinositide-3-kinase/Akt pathway

التفاصيل البيبلوغرافية
العنوان: Propofol pretreatment attenuates lipopolysaccharide-induced acute lung injury in rats by activating the phosphoinositide-3-kinase/Akt pathway
المؤلفون: L.L. Zhao, G.C. Hu, S.S. Zhu, J.F. Li, G.J. Liu
المصدر: Brazilian Journal of Medical and Biological Research, Vol 47, Iss 12, Pp 1062-1067 (2014)
بيانات النشر: Associação Brasileira de Divulgação Científica, 2014.
سنة النشر: 2014
المجموعة: LCC:Medicine (General)
LCC:Biology (General)
مصطلحات موضوعية: Acute lung injury, Propofol, Lipopolysaccharide, PI3K/Akt pathway, Medicine (General), R5-920, Biology (General), QH301-705.5
الوصف: The aim of this study was to investigate the effect of propofol pretreatment on lipopolysaccharide (LPS)-induced acute lung injury (ALI) and the role of the phosphoinositide-3-kinase/protein kinase B (PI3K/Akt) pathway in this procedure. Survival was determined 48 h after LPS injection. At 1 h after LPS challenge, the lung wet- to dry-weight ratio was examined, and concentrations of protein, tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) in bronchoalveolar lavage fluid (BALF) were determined using the bicinchoninic acid method or ELISA. Lung injury was assayed via lung histological examination. PI3K and p-Akt expression levels in the lung tissue were determined by Western blotting. Propofol pretreatment prolonged survival, decreased the concentrations of protein, TNF-α, and IL-6 in BALF, attenuated ALI, and increased PI3K and p-Akt expression in the lung tissue of LPS-challenged rats, whereas treatment with wortmannin, a PI3K/Akt pathway specific inhibitor, blunted this effect. Our study indicates that propofol pretreatment attenuated LPS-induced ALI, partly by activation of the PI3K/Akt pathway.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 1414-431X
Relation: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2014001201062&lng=en&tlng=en; https://doaj.org/toc/1414-431X
DOI: 10.1590/1414-431X20143949
URL الوصول: https://doaj.org/article/367dbc0872b44190a62f4e5f417fd854
رقم الأكسشن: edsdoj.367dbc0872b44190a62f4e5f417fd854
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:1414431X
DOI:10.1590/1414-431X20143949