Objective  To investigate the expressions of transforming growth factor-β1 (TGF-β1) and α-smooth muscle actin (α-SMA) in the lungs of mice with intra-amniotic endotoxin priming and exposed to 60% hyperoxia after born in order to elucidate the possible relationship with bronchopulmonary dysplasia (BPD).   Methods  Fifty C57 pregnant mice were divided into 2 groups: lipopolysaccharide (LPS

40 μg/L) group and saline solution group

and then received an intraamniotic injection of corresponding solution on E15. The neonatal mice of each group were randomized to be set in 60% oxygen exposure or in room air. So there were 4 subgroups

LPS+air

LPS+hyperoxia

saline+air and saline+hyperoxia groups. On days 1

3

7

10 and 14 after birth (8 rats each time point)

the lung histological changes was assessed with hematoxylin and eosin (HE) staining for radial alveolar counting (RAC). The expressions of TGF-β1 and α-SMA proteins were detected by immunohistochemical and immunofluorescence staining

and the expressions of TGF-β1 and α-SMA mRNA by real-time polymerase chain reaction (RT-PCR).   Results  In the LPS+hyperoxia group and saline+hyperoxia group

RAC began to decrease on day 3

and then further declined in a time-dependent manner. Compared with saline+hyperoxia group

LPS+hyperoxia group had significantly lower RAC (P0.05). The expression of TGF-β1 protein in LPS+hyperoxia group and saline+hyperoxia group was significantly higher than those in LPS+air group and saline+air group on day 7 (P=0.00

0.00)

which was elevated with the elapse of hyperoxia exposure time. The expression of α-SMA protein in LPS+hyperoxia group and saline+hyperoxia group was significantly higher than those in LPS+air group and saline+air group on day 7 (P=0.00

0.00)

which was increased with the increasing of hyperoxia exposure time. The changes of mRNA expression of TGF-β1 and α-SMA were basically consistent with the changes on protein expression.   Conclusion  These results suggest that the intra-amniotic endotoxin priming can enhance the effect of hyperxia exposure in up-regulating TGF-β1 and α-SMA

which may be involved in the pathogenesis of BPD.