Intravenous dexamethasone attenuated inflammation and influenced apoptosis of lung cells in an experimental model of acute lung injury
Language English Country Czech Republic Media print
Document type Journal Article
PubMed
28006948
DOI
10.33549/physiolres.933531
PII: 933531
Knihovny.cz E-resources
- MeSH
- Acute Lung Injury drug therapy metabolism pathology MeSH
- Anti-Inflammatory Agents administration & dosage MeSH
- Apoptosis drug effects physiology MeSH
- Bronchoalveolar Lavage Fluid cytology MeSH
- Dexamethasone administration & dosage MeSH
- Infusions, Intravenous MeSH
- Rabbits MeSH
- Inflammation Mediators antagonists & inhibitors metabolism MeSH
- Disease Models, Animal * MeSH
- Neutrophils drug effects metabolism MeSH
- Lung cytology drug effects metabolism MeSH
- Animals MeSH
- Check Tag
- Rabbits MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- Anti-Inflammatory Agents MeSH
- Dexamethasone MeSH
- Inflammation Mediators MeSH
Acute lung injury (ALI) is characterized by diffuse alveolar damage, inflammation, and transmigration and activation of inflammatory cells. This study evaluated if intravenous dexamethasone can influence lung inflammation and apoptosis in lavage-induced ALI. ALI was induced in rabbits by repetitive saline lung lavage (30 ml/kg, 9+/-3-times). Animals were divided into 3 groups: ALI without therapy (ALI), ALI treated with dexamethasone i.v. (0.5 mg/kg, Dexamed; ALI+DEX), and healthy non-ventilated controls (Control). After following 5 h of ventilation, ALI animals were overdosed by anesthetics. Total and differential counts of cells in bronchoalveolar lavage fluid (BAL) were estimated. Lung edema was expressed as wet/dry weight ratio. Concentrations of IL-1beta, IL-8, esRAGE, S1PR3 in the lung were analyzed by ELISA methods. In right lung, apoptotic cells were evaluated by TUNEL assay and caspase-3 immunohistochemically. Dexamethasone showed a trend to improve lung functions and histopathological changes, reduced leak of neutrophils (P<0.001) into the lung, decreased concentrations of pro-inflammatory IL-1beta (P<0.05) and marker of lung injury esRAGE (P<0.05), lung edema formation (P<0.05), and lung apoptotic index (P<0.01), but increased immunoreactivity of caspase-3 in the lung (P<0.001). Considering the action of dexamethasone on respiratory parameters and lung injury, the results indicate potential of this therapy in ALI.
References provided by Crossref.org
Early cardiac injury in acute respiratory distress syndrome: comparison of two experimental models
Acute lung injury - from pathophysiology to treatment