Protective effect of hydrogen sulfide in a murine model of acute lung injury induced by combined burn and smoke inhalation.

Abstract

Acute lung injury results in a severe inflammatory response, which leads to priming and activation of leucocytes, release of reactive oxygen and reactive nitrogen species, destruction of pulmonary endothelium, extravasation of protein-rich fluid into the interstitium and formation of oedema. Recently, H2S (hydrogen sulfide) has been shown to decrease the synthesis of pro-inflammatory cytokines, reduce leucocyte adherence to the endothelium and subsequent diapedesis of these cells from the microvasculature in in vivo studies, and to protect cells in culture from oxidative injury. In the present study, we hypothesized that a parenteral formulation of H2S would reduce the lung injury induced by burn and smoke inhalation in a novel murine model. H(2)S post-treatment significantly decreased mortality and increased median survival in mice. H2S also inhibited IL (interleukin)-1beta levels and significantly increased the concentration of the anti-inflammatory cytokine IL-10 in lung tissue. Additionally, H2S administration attenuated protein oxidation following injury and improved the histological condition of the lung. In conclusion, these results suggest that H2S exerts protective effects in acute lung injury, at least in part through the activation of anti-inflammatory and antioxidant pathways.

• Authors: Aimalohi Esechie, Levente Kiss, Gabor Olah, Eszter M Horváth, Hal Hawkins, Csaba Szabo, Daniel L Traber
• Journal: Clinical science (London, England : 1979) (Clin Sci (Lond)) Vol. 115 Issue 3 Pg. 91-7 (Aug 2008) ISSN: 1470-8736 [Electronic] England
• PMID: 18315525 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Inflammation Mediators
• Interleukin-1beta
• Interleukin-10
• Hydrogen Sulfide

Topics

• Animals
• Burns (complications)
• Disease Models, Animal
• Drug Evaluation, Preclinical
• Female
• Hydrogen Sulfide (therapeutic use)
• Inflammation Mediators (metabolism)
• Interleukin-10 (metabolism)
• Interleukin-1beta (metabolism)
• Lung (metabolism)
• Mice
• Mice, Inbred C57BL
• Oxidative Stress (drug effects)
• Respiratory Distress Syndrome (etiology, metabolism, pathology, prevention & control)
• Smoke Inhalation Injury (complications, metabolism, pathology)