Paper Title
Blockade of Arachidonic Acid Metabolites Ameliorates Reperfusion Injury of the Steatotic Liver: Evidence from Intravital Imaging of Hepatic Microcirculation

Abstract
Hepatic metabolism of arachidonic acid results in synthesis of chemically potent eicosanoid derivatives which are naturally active even in minor concentrations. High levels of arachidonic-acid derived eicosanoids, particularly thromboxane A2 (TXA2), are associated with pathological activation of coagulation and possibly generation of intravascular thrombi with provocation of intensive inflammatory response. In rodent models of fatty liver, blockade of the metabolic pathway of arachidonic acid was obtained by dietary administration of eicosapentaenoic and docosahexaenoic acids for 12 weeks. Metabolic blockade of arachidonic acid was associated with a reduced synthesis of TXA2, amelioration of hepatic microcirculation, visualized by intravital microscopy, and reduction of ischemia/reperfusion (I/R)-related hepatocellular damage. Alternatively, selective blockade of TXA2 receptors in the same mouse model achieved similar protection by single intravenous administration of selective inhibitor TXA2 receptors prior to I/R. This mini-review will focus on the effects of arachidonic acid-derived metabolites on steatotic liver I/R injury. Keywords - Arachidonic Acid, Steatotic Liver, Ischemia/Reperfusion