Role of neutrophil elastase in lung injury induced by burn–blast combined injury in rats

Abstract Objective Neutrophil elastase (NE) takes part in the pathogenesis of acute lung injury. However, its role in lung injury of burn–blast combined injury is unclear. Our objective was to assess the role of NE, and effect of sivelestat, a specific NE inhibitor, in lung injury induced by burn–bl...

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Veröffentlicht in:Burns 2013-06, Vol.39 (4), p.745-753
Hauptverfasser: Chai, Jia-ke, Cai, Jian-hua, Deng, Hu-ping, Zou, Xiao-fang, Liu, Wei, Hu, Qing-gang, Shen, Chuan-an, Yin, Hui-nan, Zhang, Xi-bo, Chi, Yun-fei, Ma, Li, Feng, Rui
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Sprache:eng
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Zusammenfassung:Abstract Objective Neutrophil elastase (NE) takes part in the pathogenesis of acute lung injury. However, its role in lung injury of burn–blast combined injury is unclear. Our objective was to assess the role of NE, and effect of sivelestat, a specific NE inhibitor, in lung injury induced by burn–blast combined injury in rats. Methods One hundred and sixty male Sprague-Dawley rats were randomly subjected to burn–blast combined injury (BB) group, burn–blast combined injury plus sivelestat treatment (S) group or control (C) group. Blood gas, protein concentration and NE activity in bronchoalveolar lavage fluid (BALF), pulmonary myeloperoxidase (MPO) activity, serum concentrations of TNF-α and IL-8, etc. were investigated from 0 h to 7 d post-injury. Results In BB group, PaO2 decreased, while NE activity in BALF, total protein concentration in BALF, pulmonary MPO activity and W/D ratio, serum concentrations of TNF-α and IL-8 increased with neutrophil infiltration, progressive bleeding and pulmonary oedema. Compared with BB group, sivelestat treatment decreased the NE activity and ameliorated the above indexes. Conclusion Sivelestat, exerts a protective effect in lung injury after burn–blast combined injury through inhibiting NE activity to decrease pulmonary vascular permeability, neutrophil sequestration, and production of TNF-α and IL-8.
ISSN:0305-4179
1879-1409
DOI:10.1016/j.burns.2012.08.005