摘要
目的检测Notch受体、AQP5、SP-C在高氧暴露下早产SD大鼠肺的表达,探讨Notch在高氧肺损伤中的作用机制。方法SD早产鼠80只随机分为对照组和高氧组,于1、71、42、1 d行肺组织病理学检查;免疫组织化学法检测Notch1、Notch3;RT-PCR检测Notch1、Notch3、AQP5S、P-C mRNA;Western blot检测AQP5、SP-C。结果病理学检查显示,高氧组肺发育滞后,Ⅱ型上皮细胞(AECⅡ)分化抑制。免疫组织化学法检测结果显示,高氧组各时间点(除7 d)肺组织Notch1表达低于对照组(P<0.05,0.01),Notch3上调(P<0.01)。Notch1、Notch3 mRNA改变类似蛋白水平。高氧组AQP5,SP-C mRNA及蛋白较对照组显著下降。结论85%高氧导致早产鼠肺Notch受体表达异常。Notch信号可能通过调控转分化参与高氧肺损伤。
Objective To observe the expression of Notchl receptor,Notch3 receptor,AQP5 and SP-C in lungs of preterm SD rats exposed to hyperoxia and explore the role of Notch in hyperoxia-induced lung injury. Methods. Preterm rats were randomly devlded into control and hyperoxia group. After 1,7,14 and 21 days ,they were used to assess lung histologic changes with HE staining and expression of Notch in lungs with immunohistochemistry. The mRNA and protein of Notchl, Notch3,AQP5, SP-C were measured by reverse transcription polymerase chain reaction （RT-PCR） and Western blot. Results Notchl mRNA levels changed similarly as histology： hyperoxia group showed lung injury characterized by inhibition of lung development. Expression of Notch in lungs： poitive staining for Notchl in hyperoxia group was much lower than that in controls （ P〈 0.01,0.05 ）, but the hyperoxia group showed higher expression of Notch3 than protein level（P〈 0.01 ）. Protein and mRNA of AQP5 and SP-C in hyperoxia group were much lower than those in controls. Conclusion Eighty-five percantye oxygen expoure results in abnormal expression of Notch receptors, which might contribute to the pathogenesis of hyperoxia induced lung injury by regulating transdifferentiation of alveolar epithelial type Ⅱ.
出处
《实用儿科临床杂志》
CAS
CSCD
北大核心
2006年第6期328-330,共3页
Journal of Applied Clinical Pediatrics
基金
国家自然科学基金项目资助(30471824)
"十五"科技攻关计划项目资助(2004BA720A11)
关键词
NOTCH
高氧症
肺损伤
早产
转分化
Notch
hyperoxia
lung injury
preterm
transdifferentiation
