高氧對發(fā)育期肺細胞凋亡和Notch1信號通路的影響
發(fā)布時間:2018-10-15 06:51
【摘要】:目的觀察高氧暴露下發(fā)育期肺組織細胞凋亡和Notch1的表達變化,探討其在新生大鼠高氧肺損傷機制中的作用。方法將120只足月SD新生大鼠隨機分為空氣組(N組)和高氧組(O組),每組60只。O組出生后立即置入氧氣(體積分數(shù))95%的持續(xù)高氧環(huán)境中飼養(yǎng),N組則在空氣中飼養(yǎng)。兩組分別于暴露高氧或空氣4、7、14d時隨機抽取8只,麻醉后取肺組織,比較兩組肺組織病理學改變、凋亡指數(shù);檢測Notch1在發(fā)育期肺組織中的表達變化。結(jié)果 O組死亡率高于N組,且O組各時間點肺組織出現(xiàn)典型的急慢性肺損傷病理學改變;TUNEL細胞凋亡檢測發(fā)現(xiàn)O組各時點細胞凋亡高于N組(P0.05);O組各時間點肺組織Notch1表達低于N組(P0.05)。結(jié)論持續(xù)高濃度氧可致肺損傷、凋亡增加和發(fā)育受阻。高氧暴露可能通過下調(diào)Notch1信號表達調(diào)控肺細胞分化發(fā)育,利于肺損傷修復。
[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.
【作者單位】: 四川大學華西第二醫(yī)院麻醉科;
【基金】:四川省科技廳科技支撐計劃項目(No.2011SZ0200)資助
【分類號】:R563
[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.
【作者單位】: 四川大學華西第二醫(yī)院麻醉科;
【基金】:四川省科技廳科技支撐計劃項目(No.2011SZ0200)資助
【分類號】:R563
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