摘要
目的观察高氧暴露下发育期肺组织细胞凋亡和Notch1的表达变化,探讨其在新生大鼠高氧肺损伤机制中的作用。方法将120只足月SD新生大鼠随机分为空气组(N组)和高氧组(O组),每组60只。O组出生后立即置入氧气(体积分数)>95%的持续高氧环境中饲养,N组则在空气中饲养。两组分别于暴露高氧或空气4、7、14d时随机抽取8只,麻醉后取肺组织,比较两组肺组织病理学改变、凋亡指数;检测Notch1在发育期肺组织中的表达变化。结果 O组死亡率高于N组,且O组各时间点肺组织出现典型的急慢性肺损伤病理学改变;TUNEL细胞凋亡检测发现O组各时点细胞凋亡高于N组(P<0.05);O组各时间点肺组织Notch1表达低于N组(P<0.05)。结论持续高浓度氧可致肺损伤、凋亡增加和发育受阻。高氧暴露可能通过下调Notch1信号表达调控肺细胞分化发育,利于肺损伤修复。
Objective To investigate the changes of lung cell apoptosis and the expression of notch signaling in the lung of neonatal rats exposed to hyperoxia and to explore the internal relationship between notch1 and hyperoxia-induced lung injury. Methods 120 neonatal Sprague-Dawley rats of 22-day gestational age were randomized continually exposed to hyperoxia（FiO2=95%,hyperoxia group）or room air（FiO2=21%,air group）30minutes after birth.The notch signaling expression in the lung were detected by immunohistochemical methods respectively at 4,7,14 days after inhale hyperoxia or air.At the same time,pathological changes in the different groups were also observed with light microscope and lung cell apoptosis was determined quantitatively by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling（TUNEL）methods.Results The biopsy test showed lung injury in hyperoxia group.The amount of apoptosis cell in hyperoxia was higer than that in the control group,and increased with the prolongation of hyperoxia supply.Positive staining for North1 in hyperoxia group was much lower than that in control group at every time point（P〈0.01,P〈0.05）.Conclusion Continually hyperoxic exposure might resulted in the lung injury and development of arrest.The abnormal expression of notch signaling might contributed to the pathogenesis of hyperoxia-induced lung injury in newborn rats.
出处
《四川大学学报（医学版）》
CAS
CSCD
北大核心
2014年第6期937-940,共4页
Journal of Sichuan University(Medical Sciences)
基金
四川省科技厅科技支撑计划项目(No.2011SZ0200)资助
关键词
NOTCH信号
发育期肺
凋亡
发育受阻
Notch signaling
Lung in development phase
Apoptosis
Lung injury
