Effect of hyperoxia on p38MAPK expression and apoptosis in the lungs of juvenile rats

李静; 许峰; 胡兰; 谭利平; 符跃强; 方芳; 匡凤梧; 卢仲毅

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Effect of hyperoxia on p38MAPK expression and apoptosis in the lungs of juvenile rats

更新时间：2026-01-09

- Effect of hyperoxia on p38MAPK expression and apoptosis in the lungs of juvenile rats
- Journal of Army Medical University Vol. 30, Issue 17, Pages: 1598-1600(2008)
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  CLC： R322.35;R329.28;R339.5
- Published：2008
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李静,许峰,胡兰,谭利平,符跃强,方芳,匡凤梧,卢仲毅.高氧对幼鼠肺组织细胞凋亡及p38 MAPK丝裂原活化蛋白激酶的影响[J].陆军军医大学学报(原第三军医大学学报),2008,30(17):1598-1600.

　LI Jing,XU Feng,HU Lan,TAN Li-ping,FU Yue-qiang,FANG Fang,KUANG Feng-wu,LU Zhong-yi.Effect of hyperoxia on p38MAPK expression and apoptosis in the lungs of juvenile rats[J].J Amry Med Univ (J Third Mil Med Univ),2008,30(17):1598-1600.
李静,许峰,胡兰,谭利平,符跃强,方芳,匡凤梧,卢仲毅.高氧对幼鼠肺组织细胞凋亡及p38 MAPK丝裂原活化蛋白激酶的影响[J].陆军军医大学学报(原第三军医大学学报),2008,30(17):1598-1600. DOI：

　LI Jing,XU Feng,HU Lan,TAN Li-ping,FU Yue-qiang,FANG Fang,KUANG Feng-wu,LU Zhong-yi.Effect of hyperoxia on p38MAPK expression and apoptosis in the lungs of juvenile rats[J].J Amry Med Univ (J Third Mil Med Univ),2008,30(17):1598-1600. DOI：

摘要

目的探讨高氧对幼鼠肺组织细胞凋亡及p38 MAPK丝裂原活化蛋白激酶表达的影响。方法幼年Wistar大鼠90％氧气暴露建立高氧肺损伤模型，行肺组织病理学检查，应用TUNEL法检测肺组织的细胞凋亡，Western blot法检测p38 MAPK表达。结果高氧暴露3 d可见肺组织水肿、出血、炎症细胞浸润等急性肺损伤改变。高氧3 d组的肺凋亡指数较空气对照组明显增加，凋亡发生的主要部位为肺泡、支气管上皮及血管内皮细胞。Western blot结果显示高氧暴露1 d，肺组织的p38MAPK活性迅速升高，于第2天达到高峰，第3天活性有所下降，但仍高于空气对照组。结论高氧暴露可以诱导肺组织发生细胞凋亡；高氧可以激活p38MAPK通路，参与高氧性肺损伤的调控；活化的p38MAPK可能参与了高氧诱导的肺组织细胞凋亡的调控。

Abstract

Objective To investigate the effect of hyperoxia on p38MAPK expression and apoptosis in the lungs of juvenile rats. Methods Thirty-two Wistar rats aged 3 weeks were divided into air exposure group and 1-day

2-day and 3-day hyperoxia exposure groups

with 8 rats in each group. The hyperoxia exposure rats were exposed to 90% O

. The resected lungs were histopathologically examined. The apoptosis and p38MAPK expressions in the resected lungs were detected by TUNEL and Western blot respectively. Results After 3-day hyperoxia exposure

the pathological changes of acute lung injury occurred

such as edema

hemorrhage and inflammatory cell infiltration. The apoptosis

index in the lungs of 3-day hyperoxia exposure group was significantly higher than that of air exposure group (P0.05)

and TUNEL showed the apoptotic cells were mainly distributed in the alveoli

airway epithelial cells and pulmonary vascular endothelial cells. Western blot results showed that p-p38 MAPK increased at the 1

day after hyperoxia

peaked at the 2

day and decreased at the 3

day. Conclusion In the course of hyperoxia-induced lung injury

high oxygen concentration can induce cell apoptosis and activiate the p38 MAPK signal pathway. The activiated p38MAPK signaling pathway may play a role in the regulation of apoptosis induced by hyperoxia.

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