摘要
目的 :研究围产期缺血缺氧对新生大鼠肺表面活性蛋白A、B(SP A ,SP B)基因表达的影响 ,探讨围产期缺血缺氧新生大鼠肺损伤机制。方法 :通过结扎孕鼠一侧子宫角血管 (其另一侧宫内胎鼠作为对照 ) ,建立围产期缺血缺氧动物模型。采用RT PCR半定量分析法观察不同程度缺血缺氧新生大鼠肺组织SP A、SP BmRNA的表达。结果 :正常 2 1d胎鼠肺组织SP A、SP BmRNA已有明显的表达 ,宫内缺血缺氧 2 0min时 ,新生大鼠肺组织SP A、SP BmRNA表达减弱 ,并随缺血缺氧时间的延长而逐渐加重。结论 :围产期缺血缺氧致新生大鼠SP A、SP
Objective: Our aims were to study the effect of the expression of surfactant protein A(SP A) and surfactant protein B(SP B) mRNA in the lung of neonatal rats following perinatal ischemic hypoxia and to investigate the mechanism of lung injury of neonatal rats after perinatal ischemic hypoxia. Methods: We set up a fetal rat model of perinatal ischemic hypoxia by ligating unilateral uterine horn vessel of pregnant Wistar rats. The pups were delivered by cesarean section at the 20 min,30 min,40 min of ischemic hypoxia. Reverse transcription polymerase chain reaction (RT PCR) was performed to evaluate relative amount of SP A and SP B mRNA expression. Results: In the rats, the expressions of SP A and SP B mRNA were very strong in normal fetal lung tissue on the 21 st day of gestation. The relative amount of SP A and SP B was reduced markedly at 20 min after ischemic hypoxia insult and reduced gradually following elongation of the insult. Conclusion: A combined reduction in gene expression of SP A and SP B may be the important mechanism of lung injury in neonatal rats after perinatal ischemic hypoxia.
出处
《中国医科大学学报》
CAS
CSCD
北大核心
2002年第2期98-100,共3页
Journal of China Medical University
