Figure 10
MaR1 improved AFC through activating the ALX/PI3K /AKT/Need4-2 pathway in vivo. MaR1 (200 ng/kg) and BOC-2 (600ng/kg), LY294002 (3 mg/kg) were co-administered to Sprague–Dawley rats through caudal vein 8 h after LPS (14 mg/kg) was administered, and intratracheal instillation of 5% albumin solution containing Evans Blue-labeled albumin (5 ml/kg) through a tracheostomy to the left lung; AFC was measured over 60 min in ventilated animals (c). Expression of phosphorylated Akt and phosphorylated SGK1 in rat lung 8 h after LPS-induced actue lung injury or saline treatment were measured by western blotting. Western blot data were replicated >3 times. The band intensity of phosphorylated Akt (a) and phosphorylated SGK1 (b) were quantitated by normalized for total Akt and total SGK1, respectively, and expressed as fold of the control. Expression of Nedd4-2 in rat lung 8 h after LPS-induced acute lung injury or saline treatment were measured by western blotting. Western blot data were replicated >3 times. The band intensity of Nedd4-2 quantitated by normalized for β-actin and expressed as fold of the control (d). Data are presented as mean±s.e.m. n=8. **P<0.01 versuscontrol group; ##P<0.01 versusLPS group; &&P<0.01 versusLPS+MaR1 group.
