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[Expression and role of p38 mitogen-activated protein kinase in hyperoxia-induced lung injury juvenile rat model]
1Intensive Care Unit, Children's Hospital, Chongqing Medical University, Chongqing, China.
Insights
Increased phosphor-p38 mitogen-activated protein kinase (p38MAPK) expression was observed in juvenile rats with hyperoxia-induced lung injury. Inhibiting p38MAPK reduced lung apoptosis, suggesting its role in this injury.
Area of Science:
- Cellular and Molecular Biology
- Pulmonary Medicine
- Toxicology
Background:
- p38 mitogen-activated protein kinase (p38MAPK) is implicated in various lung injuries.
- The role of p38MAPK in hyperoxia-induced lung injury is not well understood.
Purpose of the Study:
- To investigate the expression and role of p38MAPK in a juvenile rat model of hyperoxia-induced lung injury.
Main Methods:
- Established a hyperoxia-induced lung injury rat model using 90% O2 exposure.
- Assessed p38MAPK expression and localization via immunohistochemistry and Western blot.
- Quantified lung apoptosis using TUNEL assay and evaluated the effect of p38MAPK inhibitor SB203580.
Main Results:
- Hyperoxia exposure significantly increased phosphor-p38MAPK expression in lung tissues.
- Phosphor-p38MAPK was detected in alveolar cells, airway epithelial cells, vascular endothelium, and inflammatory cells.
- Lung apoptosis index increased significantly, and SB203580 treatment reduced both p38MAPK activation and apoptosis.
Conclusions:
- Phosphor-p38MAPK expression is upregulated in hyperoxia-induced lung injury in juvenile rats.
- p38MAPK is expressed in multiple lung cell types during injury.
- p38MAPK activation appears to contribute to apoptosis in hyperoxia-induced lung injury.
Objective:
Some research has shown that p38 mitogen-activated protein kinase (p38MAPK) plays important roles in lung injuries induced by various factors. Its expression and role in hyperoxia-induced lung injury remains unknown. This study investigated the expression and role of p38MAPK in hyperoxia-induced lung injury juvenile rat model.
Methods:
Hyperoxia-induced lung injury rat model was prepared by 90% O(2) exposure. The location and expression of p38MAPK in lung tissues were detected by immunohistochemistry and Western blot respectively. Apoptosis index of lung was evaluated by TUNEL technique. The effect of SB203580, a p38MAPK inhibitor, on the apoptosis index of lung was observed.
Results:
The expression of phosphor-p38MAPK increased obviously after hyperoxia. Positive phosphor-p38MAPK cells were mainly distributed in the alveolar, airway epithelial cells, pulmonary vascular endothelium cells and infiltrative inflammatory cells. The apoptosis index of lung also significantly elevated. SB203580 inhibited the activation of p38MAPK, and reduced the apoptosis index of lung.
Conclusions:
The phosphor-p38MAPK increased and was expressed in many kinds of lung cells in lung injury rat model. It may play a role in the induction of apoptosis in hyperoxia-induced lung injury.
