2008Di-san junyi daxue xuebaoRequires access

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

Zhong-Yi Lu

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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 (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 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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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 (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 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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Available 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 (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 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.

Key concepts: Hyperoxia, TUNEL assay, Apoptosis, Western blot, Lung, Andrology, Medicine, Biology

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