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

被引:20
|
作者
Zhao, L. L. [1 ]
Hu, G. C. [2 ]
Zhu, S. S. [1 ]
Li, J. F. [3 ]
Liu, G. J. [1 ]
机构
[1] Xuzhou Med Coll, Affiliated Hosp, Dept Anesthesiol, Xuzhou 221002, Jiangsu, Peoples R China
[2] Univ Illinois, Coll Med, Dept Pharmacol, Chicago, IL USA
[3] Tengzhou Cent Peoples Hosp, Dept Anesthesiol, Liaocheng, Shandong, Peoples R China
关键词
Acute lung injury; Propofol; Lipopolysaccharide; PI3K/Akt pathway; KERATINOCYTE GROWTH-FACTOR; PHOSPHATIDYLINOSITOL; 3-KINASE/AKT; INHIBITION; EXPRESSION; ENDOTOXIN; DEATH;
D O I
10.1590/1414-431X20143949
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
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-alpha (TNF-alpha), 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-alpha, 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.
引用
收藏
页码:1062 / 1067
页数:6
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