高氧对发育期肺细胞凋亡和Notch1信号通路的影响

发布时间：2018-10-15 06:51

【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(P0.05);O组各时间点肺组织Notch1表达低于N组(P0.05)。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。
[Abstract]:Objective to observe the changes of apoptosis and Notch1 expression in lung tissue during hyperoxia exposure and to explore its role in the mechanism of hyperoxia lung injury in neonatal rats. Methods 120 full-term SD neonatal rats were randomly divided into air group (n group) and hyperoxia group (O group). 60 rats in each group were fed with 95% oxygen (volume fraction) in continuous hyperoxic environment immediately after birth, while those in N group were fed in air. Eight lung tissues were randomly selected at 14 days after exposure to hyperoxia or air for 14 days. The pathological changes and apoptosis index of lung tissue were compared between the two groups, and the expression of Notch1 in the developing lung tissue was detected. Results the mortality of group O was higher than that of group N. The apoptosis of TUNEL cells in group O was higher than that in group N at each time point (P0.05). The expression of Notch1 in lung tissue of group O was lower than that of group N at each time point (P0.05). Conclusion continuous high oxygen concentration can induce lung injury, increase apoptosis and hinder development. Hyperoxia exposure may regulate the differentiation and development of lung cells by down-regulating the expression of Notch1 signal, which is beneficial to the repair of lung injury.
【作者单位】：四川大学华西第二医院麻醉科;
【基金】：四川省科技厅科技支撑计划项目(No.2011SZ0200)资助
【分类号】：R563

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