Objective     To study the role of chemotatic factor 12 (CXCL12)

also known as stromal cells-derived factor 1(SDF-1)

and its Cys-X-Cys receptor 4 (CXCR4)

in hyperoxia-induced lung injury and its possible mechanism.      Methods     Sixty-four Sprague-Dawley neonatal rats were randomly divided into control group and hyperoxia group. An animal model of hyperoxia-induced lung injury was established by inhaling ≥95%O

2

. After 3

7

14

and 21 days’ inhaling

the rats were killed and lung tissue samples were taken for pathological examination. Hydroxyproline level in lung tissue samples was measured with the hydrolysis method. Expression of CXCL12

CXCR4 mRNA and CXCR4 protein in lung tissue samples was detected by real-time polymerase chain reaction (RT-PCR) and Western blotting

respectively.      Results     Pathological examination showed significant inflammation and structural disorder in lung tissue of hyperoxia group. The longer the exposure to hyperoxia was

the severer the injury was. The hydroxyproline level in lung tissue samples was significantly higher in hyperoxia group than in control group after exposure to hyperoxia for 14 and 21 d（493.69±127.50 μg/g and 582.55±174.78μg/g vs 327.52±46.97μg/g and 321.27±60.63 μg/g

P0.05 or P0.01). The expression level of CXCL12 mRNA was markedly higher in hyperoxia group than in control group after exposure to hyperoxia for 14 and 21 d（2.12±1.08 and 2.68±0.87 vs 0.68±0.22 and 0.51±0.18

P0.01）. However

the expression level of CXCR4 mRNA was significantly lower in hyperoxia group than in control group（0.53±0.23

0.36±0.15 and 0.31±0.19 vs 2.80±1.14

2.71±1.26 and 2.93±0.14

P0.05）after exposure to hyperoxia for 7

14

and 21 d

while the expression level of CXCR4 protein was significantly higher in hyperoxia group than in control group after exposure to hyperoxia for 7

14 and 21 d（2.06±0.64

2.84±0.83 and 1.38±0.34 vs 1.37±0.41

0.81±0.27 and 0.85±0.23

P0.05).      Conclusion     CXCL12/CXCR4 may play an important role in inflammatory reaction and fibrosis of hyperoxia-induced lung injury.