Hou Wei, Liu Hai-Yan, Li Dan, Zhou Jian-Ping, Chen Xi
Department of Pediatrics, Second Hospital of Xi'an Jiaotong University, Xi'an 710004, China.
Zhongguo Dang Dai Er Ke Za Zhi. 2008 Apr;10(2):207-10.
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.
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.
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).
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.
血管内皮生长因子(VEGF)有助于肺发育及肺损伤后肺结构的恢复。本研究旨在探讨新生大鼠高氧肺损伤后VEGF蛋白及mRNA表达的变化。
48只Sprague-Dawley新生大鼠出生后30分钟随机持续暴露于高氧环境(FiO2 = 95%)或空气环境(FiO2 = 21%,对照组)。分别于出生后3、7和14天通过免疫组化方法及逆转录聚合酶链反应(RT-PCR)检测肺组织中VEGF蛋白及mRNA的表达。
对照组中,VEGF蛋白及mRNA表达随日龄增加而升高。与对照组相比,高氧暴露组在高氧暴露7天(7.79±5.23对12.67±3.82;P<0.01)及14天(5.85±3.37对15.10±8.91;P<0.01)时VEGF蛋白表达显著降低。与对照组相比,高氧暴露组在高氧暴露3天(0.78±0.22对1.19±0.63)至14天(0.48±0.12对1.89±0.81)时VEGF mRNA表达显著降低(P<0.01)。
VEGF与新生大鼠肺发育有关。高氧暴露可降低新生大鼠肺组织中VEGF蛋白及VEGF mRNA表达。VEGF可能参与高氧肺损伤的发病机制。