目的：血管内皮生长因子（VEGF）参与肺的发育和损伤修复，VEGF具有促进肺泡和肺血管增殖以及预防新生儿支气管肺发育不良（BPD）的作用。该研究的目的是探讨新生大鼠高氧肺损伤后肺组织VEGF蛋白及VEGF mRNA表达的变化。方法：新生Sprague-Dawley大鼠48只随机分为高氧实验组和空气对照组，高氧实验组吸入95%以上高氧建立高氧肺损伤模型。分别采用免疫组化法和逆转录多聚酶链式反应（RT-PCR）检测新生大鼠3 d，7 d，14 d肺组织VEGF蛋白及VEGF mRNA表达变化。结果：空气对照组新生大鼠生后随着肺发育，肺组织中VEGF蛋白及VEGF mRNA表达逐渐增加。高氧实验组新生鼠吸入高氧3 d，肺VEGF蛋白表达出现降低，在7 d，14 d明显降低与对照组比较差异有显著性（VEGF 蛋白:12.67±3.82 vs 7.79±5.23; 15.10±8.91 vs 5.85±3.37, 均P<0.01）；高氧实验组VEGF mRNA表达在3 d，7 d，14 d均明显低于对照组（VEGF mRNA: 1.19±0.63 vs 0.78±0.22, 1.52±0.47 vs 0.53±0.18, 1.89±0.81 vs 0.48±0.12, 均P<0.01）。结论：VEGF能促进新生大鼠肺发育，VEGF蛋白及VEGF mRNA表达与新生大鼠肺发育有密切关系。高氧可抑制VEGF蛋白及VEGF mRNA在新生大鼠肺内的表达，VEGF在新生鼠肺发育和高氧肺损伤发病机制中起重要作用。

OBJECTIVE: Vascular endothelial growth factor (VEGF) contributes to lung development and recovery of lung structure from lung injury. This study aimed to explore the changes of expression of VEGF protein and mRNA in neonatal rats following hyperoxic lung injury. METHODS: Forty-eight Sprague-Dawley neonatal rats were randomly continually exposed to hyperoxia (FiO2=95%) or to room air (FiO2=21%, control group) 30 minutes after birth. VEGF protein and mRNA expression in the lungs was determined by immunohistochemical methods and reverse tanscription polymerasechain reaction (RT-PCR) respectively 3,7 and 14 days after birth. RESULTS: VEGF protein and mRNA expression increased with increasing postnatal age in the control group. In the hyperoxia exposure group VEGF protein expression decreased markedly at 7 days (7.79±5.23 vs 12.67±3.82; P<0.01) and 14 days of hyperoxia exposure (5.85±3.37 vs 15.10±8.91; P<0.01) compared with the controls. VEGF mRNA expression in the hyperoxia exposure group was significantly reduced from 3 days (0.78±0.22 vs 1.19±0.63) through 14 days of hyperoxia exposure (0.48±0.12 vs 1.89±0.81) compared with the controls (P<0.01). CONCLUSIONS: VEGF is associated with lung development in neonatal rats. Hyperoxia exposure can decrease VEGF protein and VEGF mRNA expression in the lungs of neonatal rats. VEGF might be involved in the pathogenesis of hyperoxic lung injury.