| PrefaceBronchopulmonary dysplasia ( 8PD) is the most common form of chronic lung disease (CLD)in neonates. At present the pathogenic mechanisms of BPD is imperfect and likely involves oxidant injury barotraumas and premature birth. Recent years,the role of grow factor in hyperoxia - induced lung injury was increasingly reconstred, and vascular endothelial growth factor (VEGF) in hyperoxia - induced lung injury are becoming new focus of much interest and debate. VEGF may also be necessary for endothelial cell survival, particularly inhyperox-ic conditions. Previous studies of BPD have generally focused on abnormalities of precapillary arterioles and the development of alveolar abnormalities,However, little is known about grow factor in this disease and lack the development observation. In the experimentwe measured VEGF expression of the level protein and molecular in prolong hyperoxia, in neonatal mice lung using immunohistochemis-try and In Situ hybridization. The purpose of study is to provid powerful experiment base to deeply approach mechanism of BPD.Methods and materials1. Establishment of animal model; newborn pups from four to eight litters ( about 40 ~50 pups pre group) were pooled before being randomly redistributed to oxygen - exposed group and room air group, the newborn pups of Oxygen -expoused group were placed in Plexiglas chambers into which oxygen was continuously delivered. Continuous flow achieved a constant level of 90% oxygen.2. Five pups from each group were killed after 1,2,3,7,14,21 days of oxygen exposure, lung tissue were fixed in situ with 4% paraformaldehyde.3. After lung tissue sections were stained with hematoxylin and eosin (H&E) , pathologic chang was observed under light microscope.4. Expression of VEGF protein was detected in immunohistochemistry.5. Expression of VEGF mRNA was detected in In Situ hybridization.6. Statistical analysis: Data were expressed as mean SD values. Results were compared with Dunnett t test.Result1. Lung pathology examination: Neonatal hyperoxia resulted in descreased alveolar septation, lung micrangium dysplasia and interstitial fibrosis. theses chang were obviouse after seven days and furthermore predominance after 14 and 21 days.2. Expression of VEGFmRNA and protein was prominent in alveolar septa. VEGF protein was also localized in vascular smooth muscle and some bronchial epithelial.3. Expression of VEGFmRNA and protein was singnificantly decreased during hyperoxia in neonatal mice( P <0.01).DiscussionVEGF is a relatively specific endothelial cell mitoen that regulates endothe-lial cell proliferation ?differentiation, capillary permeability and angiogensis . In lung,VEGF mainly expresses in the distal epithelium and modulates activity in adjacent vascularendothelium as a paracrine mediator. Our study find that neonatal hyperoxia resulted in descreased alveolar septation, lung micrangium dysplasia and interstitial fibrosis. theses chang were obviouse after seven days and furthermore predominance after 14 and 21 daysExpression of VEGFmRNA and protein was prominent in alveolar septa. VEGF protein was also localized in vascular smooth muscle and some bronchial epithelial; Expression of VEGFmRNAand protein was singnificantly decreased during hyperoxia in neonatal mice( P < 0.01). Our result suggest that decreased VEGF of prolongeds hyperoxia in neonatal mice is an important factor of the development of BPD. The role of VEGF is still imperfect in BPD. Recently, it has been considered that decreased VEGF relates to apoptosis of vascular endothelial cell during exposed to hyperoxia. VEGF maintains endothelial cell survival through interfering apoptosis. Decreased VEGF during exposed to hyperoxia may be destroy the surviva of endothelial cell and trigger apoptosis, thereby lead to rnicrangium dysplasia in BPD. A potential mechanism of decreased VEGF expression in BPD is a change in the cell pheno-type of alveolar epithelial cells. VEGF - expressing type II cells may have been displaced by high SP - C - e...
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