Role of p38MAPK in hyperoxia-induced lung injury of newborn rats

Objective To investigate the expression of p38MAPK and the mechanism of lung protective effect of its specific inhibitor SB203580 in newborn rats with hyperoxia induced lung injury. Methods One hundred and sixty newborn rats were divided randomly into 4 group: Ⅰ air control group, Ⅱ hyperoxia induced lung injury group, Ⅲ hyperoxia induced lung injury + SB203580 group (intraperitoneal injection at 5 mg/kg, 1/d, totally 3 days) and Ⅳ hyperoxia induced lung injury + Sodium Chloride group.Group Ⅱ, Ⅲ and Ⅳ were exposured to hyperxia (95%) for 72 h, at the same time, group Ⅰ were fed in normal air . The rats were sacrificed 12 h, 24 h, 72 h and 1 week after hyperoxia and SB203580 treatment. Right upper lobe of lungs were harvested for histopathologic study, right lower lobe of lungs were harvested for measurement of wet/dry weight (W/D) ratio and left lung were harvested for measurement of expression of p38MAPK by Western blot and TGF-β1 concentration by ELISA. Results The expression of p38MAPK was strongly positive in hyperoxia group and hyperoxia + Sodium Chloride group at 72 hours. In these groups, the concentration of TGF-β1 increased significantly with time lasting and their concentrations were higher than those in the air control group and hyperoxia + SB203580 group at each time point (P0.01). Conclusions p38MAPK is involved in the process of hyperoxia induced lung injury. The lung injury can be relieved by administering SB203580 which blocks the expression of p38MAPK, then inhibiting the expression of TGF-β1.