Lipoxin receptor agonist, may be a potential treatment for hemorrhagic shock-induced acute lung injury

Med Hypotheses. 2012 Jul;79(1):92-4. doi: 10.1016/j.mehy.2012.04.010. Epub 2012 Apr 29.

Abstract

The main pathogenesis of acute lung injury induced by hemorrhagic shock is increasingly recognized as an inflammatory process. BML-111, a lipoxin receptor agonist, has been demonstrated to promote acute inflammatory resolution by reduction of pro-inflammatory cytokines, attenuation of neutrophilic infiltration, and increasing macrophage phagocytosis of apoptotic neutrophils. Meanwhile, lipoxins and lipoxin analogues have been reported to play pro-resolving and anti-inflammatory effects in many disease models including cerebral ischemia, dorsal air pouch, peritonitis, and so on. Therefore, we hypothesize that BML-111 may be implicated in pathogenesis of hemorrhagic shock-induced acute lung injury.

Publication types

  • Randomized Controlled Trial
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acute Lung Injury / drug therapy*
  • Acute Lung Injury / etiology
  • Animals
  • Rats
  • Receptors, Lipoxin / agonists*
  • Shock, Hemorrhagic / complications
  • Shock, Hemorrhagic / drug therapy*

Substances

  • Receptors, Lipoxin