BML-111, a lipoxin receptor agonist, protects haemorrhagic shock-induced acute lung injury in rats.
Jie Gong, Si Guo, Hong-Bin Li, Shi-Ying Yuan, You Shang, Shang-Long Yao
Department of Anesthesiology and Critical Care, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Resuscitation 2012 JulThe main pathogenesis of acute lung injury induced by haemorrhagic shock is inflammation. BML-111, a lipoxinA(4)-receptor agonist, promotes acute inflammatory resolution. We sought to elucidate whether BML-111 protects haemorrhagic shock-induced acute lung injury in rats. Thirty two adult male rats were randomized to sham group (sham), haemorrhagic shock/resuscitation (HS), HS plus BML-111 (BML-111), and HS plus BML-111 and BOC-2 (BOC-2). Haemorrhagic shock was induced by blood drawing, and then resuscitation was obtained by infusion of shed blood and two-fold volume saline. Histological findings, as well as assays of neutrophilic infiltration (myeloperoxidase activity, ICAM-1 expression), inflammatory cytokines and pro-inflammatory factor (IκB-α and NF-κB p65) confirmed that haemorrhagic shock induced acute lung injury. BML-111 significantly mitigated acute lung injury induced by haemorrhagic shock. However, BOC-2, an antagonist of the lipoxinA(4)-receptor, partially reversed the protective effect of BML-111 on the haemorrhagic shock-induced the acute lung injury. BML-111 protects haemorrhagic shock-induced acute lung injury in rats. Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.
Citation
Jie Gong, Si Guo, Hong-Bin Li, Shi-Ying Yuan, You Shang, Shang-Long Yao. BML-111, a lipoxin receptor agonist, protects haemorrhagic shock-induced acute lung injury in rats. Resuscitation. 2012 Jul;83(7):907-12
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PMID: 22245750
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