Figure 6
PD98059 reduced the effects of hyperoxia on high-tidal volume (VT)-induced ERK1/2 activation. The mice ventilated at a VT of 30 ml/kg (VT 30 ml) with or without hyperoxia were pretreated with 1 mg/kg PD98059 for 30 minutes. (a) Phosphorylated ERK1/2 expression (top panel), total ERK1/2 protein expression (middle panel), and quantitation by arbitrary units (bottom panel) (n = 5 per group). The relative phosphorylation was expressed in arbitrary units. (b) Representative photomicrographs (×400) with phospho-ERK1/2 staining of the lung sections (n = 5 per group). (A) Control wild-type mice with room air. (B) Control wild-type mice with hyperoxia. (C) Wild-type mice ventilated at a VT of 30 ml/kg with room air. (D) Wild-type mice ventilated at a VT of 30 ml/kg with hyperoxia. (E) Mice pretreated with PD98059 and ventilated at a VT of 30 ml/kg with room air. Positive staining of airway epithelia is identified by arrows. (F) Mice pretreated with PD98059 and ventilated at a VT of 30 ml/kg with hyperoxia. Phospho-ERK1/2-positive cells were quantified as the average number of epithelial cells with dark brown DAB signals per bronchiole, which were counted from 10 randomly chosen bronchioles of each section (n = 5 per group). *p < 0.05 versus control, non-ventilated mice; †p < 0.05 versus all other groups. DAB, diaminobenzidine; ERK, extracellular signal-regulated kinase; O2, mice with hyperoxia; RA, mice with room air; WT, wild-type mice.