Objective:To explore distributions and expressions of ERK

JNK

p38 MAP kinase in lung tissues and roles of MAP kinases on hyperoxia-induced lung injury with signal pathway inhibitors. Methods:Sixty Wistar rats aged 3 weeks old were randomized to 10 groups with 6 rats in each:room-air group(A)

hyperoxia exposure 3

7

14 days groups(O3

O7

O14)

hyperoxia 7 d+ PD98059 group (O7+PD)、hyperoxia 7 d +SB203580 group(O7+SB)

hyperoxia 7 d+ SP600125 group(O7+SP) and room-air +inhibitors groups.Rats had received i.v injection of PD98059(0.3 mg/kg)and SB203580(0.2 mg/kg) and injected with SP600125(15 mg/kg) intraperitoneally.Lung pathology examined by light microscopy

lung wet/dry ratio(W/D) and protein level in BALF and permeability coefficient were evaluated.The location and quantity of MAP kinases protein were detected by immunohistochemistry and Western blot analysis respectively.Results:Lung injury in hyperoxia exposure groups were developed as compared with room-air group

W/D and protein level in BALF and permeability coefficient in O7 and O14 groups were increased than those in control group(P<0.05)

lung tissue pathology in O7+SB and O7+SP groups were improved than that in O7 group

as evidenced by decreased pathology score and decreased W/D

total protein in BALF and permeability coefficient(P<0.05).The positive cells remarkably increased in hyperoxia groups andthe positive cells labeled in many types cells.MAP kinases positive cells in inhibitors groups decreased significantly.Protein quantity of ERK

p38

JNK in hyperoxia exposure groups were remarkablely higher than those in room-air group

protein expression of ERK in O7 group and p38 in O14 group and JNK in O14 group were strongest in all hyperoxia groups.Signal inhibitors could inhibit corresponding MAP kinases protein expression.Conclusion:High concentration of oxygen activated ERK

p38

JNK signaling pathway in lung tissue

p38 and JNK may exert promotion role on hyperoxia induced lung injury development.