Abstract
Objective To investigate the changes of VEGF and its receptor, fetal liver kinase-1 (Flk-1) expression, in lungs of premature rats exposed to 60% oxygen and elucidate the relationship between O2 exposure and the pathogenesis of bronchopulmonary dysplasia (BPD). Methods Midoxygen lung injury model was established by exposing to 60% O2 in the preterm period of Spraque Dawley rats. Rats exposed to air were used as control group. At day 1, 4, 7, 11 and 14 after birth, the lungs from each subjects were removed and dissected from the main bronchi for analysis. Eight rats of each group were used to assess lung histologic changes with HE staining. Lung VEGF and its receptor Flk-1 mRNA and protein levels were measured by reverse transcription polymerase chain reaction (RT-PCR) and western blot. Results (1) Radial alveolar counts in mid-oxygen group was 8.23±0.11 at day 7, 8. 53±0.08 at day 11 and 9. 03±0.17 at day 14, lower than control group(P〈 0. 05). (2)VEGF mRNA, Flk-1 mRNA and protein level in mid-oxygen group were lower than control group at day 7, 11 and 14 (P〈0.05). (3) The VEGF164 protein levels in mid-oxygen group were found to decrease at day 11 and 14 comparing with control group (P〈0.05). Conclusions Changes of the expression of VEGF and its receptor Flk-1 in lungs of premature rats exposed to 60% oxygen may contribute to the development of BPD. Key words: Hyperoxia; Bronchopulmonary dysplasia; Vascular endothelial growth factor A; Vascular endothelial growth factor receptor-2; Rats; Infant, premature
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