Propofol pretreatment attenuates lipopolysaccharide-induced acute lung injury in rats by activating the phosphoinositide-3-kinase/Akt pathway
AUTOR(ES)
Zhao, L.L., Hu, G.C., Zhu, S.S., Li, J.F., Liu, G.J.
FONTE
Braz J Med Biol Res
DATA DE PUBLICAÇÃO
14/10/2014
RESUMO
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.
Documentos Relacionados
- Galantamine protects against lipopolysaccharide-induced acute lung injury in rats
- Transcriptional Profiling of Lipopolysaccharide-Induced Acute Lung Injury
- Propofol exerts anti-inflammatory effects in rats with lipopolysaccharide-induced acute lung injury by inhibition of CD14 and TLR4 expression
- v-Crk activates the phosphoinositide 3-kinase/AKT pathway in transformation
- Exogenous normal lymph alleviates lipopolysaccharide-induced acute lung injury through lessening the adhesion molecules