粘着斑激酶在早产大鼠高氧肺损伤肺组织中的表达变化和意义

目的探讨粘着斑激酶(FAK)与高氧肺损伤发生、发展的关系。方法剖宫术取出孕21 d大鼠作为早产鼠,分别置早产鼠于85％高氧环境下3、7和14 d,各组均以空气组早产鼠为对照,留取肺组织标本,采用免疫组织化学法和Western blot技术对高氧组和空气组肺组织FAK多肽表达进行定位、定量检测,采用RT-PCR方法对FAK mRNA表达水平进行半定量分析。结果 FAK mRNA和蛋白在空气组早产大鼠肺组织均有较高水平表达,高氧暴露3、7和14 d后,FAK mRNA和蛋白表达水平均呈不同程度的下降,尤以高氧14 d最明显。结论高氧抑制FAK表达是导致正常肺泡化过程受阻以及不成熟肺组织损伤后异常修复的重要因素,其机制可能与其抑制肺泡上皮细胞增殖、分化,以及毛细血管形成有关。

Role of hyperoxia on the expression of focal adhesion kinase in lung tissues of premature rat

Objective To explore the role of hyperoxia on the expression of focal adhesion kinase (FAX) in lung tissues of premature rats. Methods One-day-old preterm rats were randomly assigned to the air group (exposed to room air continuously) and the hyperoxia group (exposed to 85% oxygen continuously) .The lung tissue in two groups was obtained at 3, 7 and 14 days after exposing to either room air or hyperoxia. FAK mRNA and FAX were detected by RT-PCR, immunohistochemistry and Western blot, respectively. Results Comparing to the air group, the expression of FAK mRNA and the synthesis of FAX all decreased markedly in hyperoxia groups at day 3 (F<0.05), day 7 (P<0.05) and day 14 (P<0.01), respectively. Conclusions It is suggested that the decreased expression of FAK induced by hyperoxia is likely to contribute to the pathogenesis of hyperoxic lung injury and the inhibition of premature lung development through probably the inhibition of alveolar epithelial proliferation, differentiation and blood capillary morphogenesis.