Study of cyclooxygenase-2 in renal ischemia-reperfusion injury

The pathogenesis of ischemia-reperfusion (I/R) injury is known to involve cytokines and particularly surface adhesion molecules, the expression of which initiates the attachment of inflammatory cells. Cyclooxygenase (COX)-l and COX-2 catalyze the initial key enzymatic steps in the metabolism of arachidonic acid. COX-1 is constitutively expressed in most tissues, whereas COX-2 is induced in response to proinflamamatory cytokines and stress. In this study we examined the expression of COX-1 and COX-2 in the rat after 90 minutes of warm-I/R injury. Rats were sacrificed at 0, 1.5, 3, 5, 12, and 24 hours after reperfusion. COX-2 expressions were analyzed by immunohistochemical staining, which was graded on a scale of 0 to 4. All results are presented as the mean values +/- SD. Data analyses used analysis of variance. COX-2 expression was most intense on endothelial cells at 3 and 5 hours after reperfusion. From 12 to 24 hours after reperfusion COX-2 expression on endothelial cells gradually became weaker. COX-2 expression scores were significantly higher at 1.5, 3, 5, 12, and 24 hours after reperfusion than at 0 hours. However, there were no differences in COX-1 expression after reperfusion. Several hours after the maximum of COX-2 expression the maximum renal I/R injury was observed. These results suggest a relationship between COX-2 expression and renal I/R injury.