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[Edaravone has a protective role in a mouse model of pulmonary oxygen toxicity]
Xiao-Chen Bao1, Yi-Qun Fang1, Jun Ma1
1Department of Diving Medicine, Naval Medical Research Institute, Shanghai 200433, China.
Objective:
To find if edaravone can play a protective role in a mouse model of pulmonary oxygen toxicity and explore the intervention mechanism.
Methods:
Thirty male C57BL/6 mice were randomly divided into 3 groups(Air +Vehicle, Hyperbaric oxygen(HBO) +Vehicle and HBO + Edaravone). Mice were either given edaravone (5 mg/(kg·d)) in sterilized water or a sterilized water vehicle for 3 days before oxygen exposure. Mice in HBO groups were exposed to 0.23 MPa hyperoxia (≥95% O2) for 6 h. Lung tissues were collected and the wet/dry ratio of lung were analyzed. For histologic analysis, lung sections were stained with hematoxylin and eosin (HE). Proinflammatory cytokine levels and antioxidant enzyme activities in lungs were determined by using ELISA kits. The expression levels of pro-apoptosis protein were determined with Western blot analysis.
Results:
Edaravone treatment could significantly reduce lung permeability, decrease tissue pro-apoptosis protein (cleaved-caspase3) and inflammation (IL-1β). However, edaravone treatment had no effect on antioxidant enzyme activities.
Conclusion:
These results showed that edaravone treatment had a protective role in pulmonary oxygen toxicity through curbing inflammation and apoptosis.
Insights
Edaravone protects against pulmonary oxygen toxicity by reducing inflammation and apoptosis in mice. This study explored its protective role and intervention mechanisms in a relevant animal model.
Area of Science:
- Pulmonary Medicine
- Toxicology
- Pharmacology
Background:
- Pulmonary oxygen toxicity is a significant clinical concern.
- Understanding protective mechanisms against hyperoxia is crucial.
Purpose of the Study:
- To investigate the protective effects of edaravone in a mouse model of pulmonary oxygen toxicity.
- To elucidate the underlying intervention mechanisms of edaravone.
Main Methods:
- Mice were exposed to hyperbaric oxygen (HBO) and treated with edaravone or vehicle.
- Lung permeability, inflammation, apoptosis markers, and antioxidant enzyme activity were assessed.
- Histological analysis and Western blot were employed.
Main Results:
- Edaravone significantly reduced lung permeability and decreased levels of pro-apoptosis protein (cleaved-caspase-3) and inflammation (IL-1β).
- Edaravone did not affect antioxidant enzyme activities in the lung tissue.
Conclusions:
- Edaravone demonstrates a protective role in mitigating pulmonary oxygen toxicity.
- The protective effects are attributed to the suppression of inflammation and apoptosis.
