Budesonide ameliorates lung injury induced by large volume ventilation

BMC Pulm Med. 2016 Jun 4;16(1):90. doi: 10.1186/s12890-016-0251-z.

Abstract

Background: Ventilation-induced lung injury (VILI) is a health problem for patients with acute respiratory dysfunction syndrome. The aim of this study was to investigate the effectiveness of budesonide in treating VILI.

Methods: Twenty-four rats were randomized to three groups: a ventilation group, ventilation/budesonide group, and sham group were ventilated with 30 ml/kg tidal volume or only anesthesia for 4 hor saline or budesonide airway instillation immediately after ventilation. The PaO2/FiO2and wet-to-dry weight ratios, protein concentration, neutrophil count, and neutrophil elastase levels in bronchoalveolar lavage fluid (BALF) and the levels of inflammation-related factors were examined. Histological evaluation of and apoptosis measurement inthe lung were conducted.

Results: Compared with that in the ventilation group, the PaO2/FiO2 ratio was significantly increased by treatment with budesonide. The lung wet-to-dry weight ratio, total protein, neutrophil elastase level, and neutrophilcount in BALF were decreased in the budesonide group. The BALF and plasma tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, intercellular adhesion molecule (ICAM)-1, and macrophage inflammatory protein (MIP)-2 levels were decreased, whereas the IL-10 level was increased in the budesonide group. The phosphorylated nuclear factor (NF)-kBlevels in lung tissue were inhibited by budesonide. The histological changes in the lung and apoptosis were reduced by budesonide treatment. Bax, caspase-3, and cleaved caspase-3 were down-regulated, and Bcl-2 was up-regulated by budesonide.

Conclusions: Budesonide ameliorated lung injury induced by large volume ventilation, likely by improving epithelial permeability, decreasing edema, inhibiting local and systemic inflammation, and reducing apoptosis in VILI.

Keywords: Budesonide; Lung injury; Mechanical ventilation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / drug effects
  • Bronchoalveolar Lavage Fluid / chemistry
  • Bronchoalveolar Lavage Fluid / cytology
  • Budesonide / therapeutic use*
  • Caspase 3 / blood
  • Caspase 3 / chemistry
  • Chemokine CXCL2 / blood
  • Chemokine CXCL2 / chemistry
  • Glucocorticoids / therapeutic use*
  • Intercellular Adhesion Molecule-1 / blood
  • Intercellular Adhesion Molecule-1 / chemistry
  • Interleukin-10 / blood
  • Interleukin-10 / chemistry
  • Interleukin-1beta / blood
  • Interleukin-1beta / chemistry
  • Interleukin-6 / blood
  • Interleukin-6 / chemistry
  • Leukocyte Count
  • Lung / physiopathology*
  • Male
  • NF-kappa B / chemistry
  • Proto-Oncogene Proteins c-bcl-2 / chemistry
  • Random Allocation
  • Rats
  • Rats, Wistar
  • Respiration, Artificial / adverse effects*
  • Tidal Volume
  • Tumor Necrosis Factor-alpha / blood
  • Tumor Necrosis Factor-alpha / chemistry
  • Ventilator-Induced Lung Injury / drug therapy*
  • bcl-2-Associated X Protein / chemistry

Substances

  • Bax protein, rat
  • Chemokine CXCL2
  • Cxcl2 protein, rat
  • Glucocorticoids
  • Interleukin-1beta
  • Interleukin-6
  • NF-kappa B
  • Proto-Oncogene Proteins c-bcl-2
  • Tumor Necrosis Factor-alpha
  • bcl-2-Associated X Protein
  • Intercellular Adhesion Molecule-1
  • Interleukin-10
  • Budesonide
  • Casp3 protein, rat
  • Caspase 3