高氧致慢性肺疾病早产鼠肺组织水通道蛋白-5及表面活性蛋白-A、B基因表达的意义  

Expressions of Surfactant Protein A,B and Aquaporin-5 mRNA in Premature Rats with Hyperoxia-Induced Chronic Lung Disease and Those Significances

作　　者：富建华[1] 于凤英[1] 潘丽[1] 薛辛东[1] 

机构地区：[1]中国医科大学附属盛京医院儿科,沈阳110004

出　　处：《实用儿科临床杂志》2007年第22期1731-1733,共3页Journal of Applied Clinical Pediatrics

基　　金：国家自然科学基金项目资助(30672253)

摘　　要：目的探讨慢性肺疾病(CLD)早产鼠肺上皮细胞特异性标志物表面活性蛋白A、B(SP-A、SP-B)通道蛋白-5(AQP5)基因表达规律及其意义。方法将80只早产鼠随机分为模型和对照组(每组40只),采用高体积分数氧诱导慢性肺疾病模型,于实验后1、3、7、14、21d应用反转录聚合酶链式反应(RT-PCR)检测其肺组织SP-A、SP-B及AQP5mRNA表达。结果生后初期2组SP-A、SP-B及AQP5均无统计学差异(Pa>0.05),7d实验组SP-A及SP-B明显高于对照组(Pa<0.05),14d时显著高于对照组(Pa<0.01),21d时仍明显高于对照组(Pa<0.05);同时间点与对照组比较,AQP5均维持在较低水平(Pa<0.05)。结论高体积分数氧诱导早产鼠的Ⅱ型肺泡上皮细胞(AEC-Ⅱ)向Ⅰ型肺泡上皮细胞(AEC-Ⅰ)分化障碍可能是CLD肺上皮修复异常的重要机制。Ohjeetive To explore the dynamic changes of expressions of suffaetant protein A, B （ SP - A, B） and aquaporin5 （ AQP5 ） mRNA of specificity mark in alveolar epithelial cell（AEC） of premature rats with chronic lung disease （CLD） and those signifieanees. Methods Eighty premature rats were randomly and equally divided into model group（ hyperoxia group） and control group（ room air group）. CLD was induced by hyperoxia exposure. The gene expressions of SP - A, SP - B and AQP5 were assayed with reverse transcription polymerase chain reaction （ RT - PCR） after 1,3,7,14 and 21 days. Results Compared with control group,in hyperoxia group,the levels of SP- A and SP- 13 mRNA increased from day 7 （ Pa 〈 0.05 ） , remained higher on day 14 （ P 〈 0.01 ） , and reached the peak on day 21 （ Pa 〈 0.05 ）. Level of AQP5 mRNA were lower than that of the control group on days 7,14 and 21 （ Pa 〈 0.05 ）. Conclusion The differentiation disorder from type Ⅱ AEC to type Ⅰ AEC may play an important role in inhibition of lung development with CLD.

关 键 词：表面活性蛋白 水通道蛋白 肺泡上皮细胞 分化 高氧 

分 类 号：R722.6[医药卫生—儿科]