[1]李静,许峰,胡兰,等.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,et al.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.
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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(/HTML )
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陆军军医大学学报(原第三军医大学学报)[ISSN:1000-5404/CN:51-1095/R]

卷:
30卷
期数:
2008年第17期
页码:
1598-1600
栏目:
论著
出版日期:
2008-09-15

文章信息/Info

Title:
Effect of hyperoxia on p38MAPK expression and apoptosis in the lungs of juvenile rats
作者:
李静许峰胡兰谭利平符跃强方芳匡凤梧卢仲毅
重庆医科大学附属儿童医院ICU
Author(s):
LI Jing XU Feng HU Lan TAN Li-ping FU Yue-qiang FANG Fang KUANG Feng-wu LU Zhong-yi
Intensive Care Unit, Children’s Hospital, Chongqing Medical University, Chongqing 400014, China
关键词:
高氧细胞凋亡p38 MAPK丝裂原活化蛋白激酶
Keywords:
hyperoxia cell apoptosis p38 mitogen-activated protein kinase
分类号:
R322.35; R329.28; R339.5
文献标志码:
A
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% O2. 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 (P<0.05), 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 1st day after hyperoxia, peaked at the 2nd day and decreased at the 3rd 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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更新日期/Last Update: 2008-09-16