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The metabolism of arachidonic acid by either the cyclooxygenase (COX) or the lipoxygenase (LOX) pathway generates eicosanoids, which have been implicated in the pathogenesis of a variety of human diseases, including ischemia-reperfusion (I/R) injury. Several reports have demonstrated that COX-2 and LOX inhibitors can reduce the damage caused by I/R injury. However, few reports have investigated the effects of COX and LOX expression on renal I/R injury, thus this study aimed to do so in a rat renal I/R injury model. The right kidney was harvested and the left renal artery and vein were clamped under laparotomy. The kidney was reperfused after 90 min of ischemia, and rats were sacrificed at 0, 1.5, 3, 5, 12 and 24 h after reperfusion. COX and LOX expression was analyzed by immunohistochemistry. COX-2 and 5- and 12-LOX expression was most intense in the endothelial cells at 3 and 5 h after reperfusion. The expression of COX-2 was stronger than that of 5- and 12-LOX. However, in the hours following reperfusion there were no significant variations in COX-1 expression. Our results demonstrate that COX-2 and LOX can be induced in a rat renal I/R injury model, and that the arachidonic acid pathways play a very important role in renal I/R injury.

The role of arachidonic acid in a rat renal ischemia-reperfusion injury model