临床儿科杂志 ›› 2014, Vol. 32 ›› Issue (4): 355-359.

• 实验研究 • 上一篇    下一篇

血管生成素-1在高氧诱导新生鼠支气管肺发育不良的表达及与肺发育的关系

王玲,吕回,李美雪   

  1. 广州市妇女儿童医疗中心新生儿科(广东广州 510120)
  • 收稿日期:2013-11-09 出版日期:2014-04-15 发布日期:2014-04-15

Expression of angiopoietin-1 and lung development in neonatal rat with hyperoxia-induced BPD 

WANG Ling, LU Hui, LI Meixue    

  1. (Department of Neonatology, Guangzhou Women and Children's Medical Center, Guangzhou 510120, Guangdong, China)
  • Received:2013-11-09 Online:2014-04-15 Published:2014-04-15

摘要:

 目的 探讨血管生成素(Ang-1)在高氧诱导支气管肺发育不良(BDP)新生大鼠中的表达。方法 48只生后2~3日龄的新生大鼠随机分为高氧组和对照组,每组24只,分别置于高氧(氧浓度≥95%)和空气中持续喂养;于高氧暴露第1、3、7天,光镜下观察大鼠肺组织形态结构变化,并采用实时荧光定量PCR和Western blotting方法分别检测大鼠肺组织中Ang-1 mRNA和蛋白表达水平。结果 随着高氧暴露时间延长,光镜下高氧组逐渐表现出肺组织发育不良、肺泡结构简单化、肺泡数目减少和肺微血管发育受阻等病理改变。高氧暴露第7天,高氧组的Ang-1 mRNA和蛋白相对表达为0.33±0.18和0.20±0.07,低于对照组的0.83±0.46和0.57±0.44,差异有统计学意义(P均<0.05)。结论 Ang-1是肺血管发育过程中的重要调节因子,参与了BPD病理发生。

Abstract:  Objective To explore the expression of angiopoietin-1 (Ang-1) and lung development in neonatal rat with hyperoxia-induced bronchopulmonary dysplasia (BPD). Methods A total of forty-eight 1- to 3-day-old neonatal rats were randomly divided into hyperoxia group and control group with 24 rats in each group, fed in high concentration oxygen (≥95%) or in air respectively. At 1st, 3rd and 7th day after high oxygen exposure, the histological changes in lung tissue were observed by HE stai-ning under a light microscope and the expressions of Ang-1 mRNA and its protein in lung tissue were detected by RT-PCR and Western blot. Results With extended exposure to high concentrations of oxygen, rats in hyperoxia group presented such pathologic change of lung tissue dysplasia as alveolar simplification, reduction in alveolar number and arrested pulmonary microvascular development. At 7th day after high oxygen exposure, Ang-1 mRNA and protein expressions in hyperoxia group were (0.33±0.18) and (0.20±0.07), significantly lower than those [(0.83±0.46) and (0.57±0.44)] in control group (P<0.05). Conclusions Ang-1 plays an important regulatory role in the pulmonary vascular development and participates in the pathogenesis of BPD.