Inhibition of COX in Ocular Tissues: AnIn VitroModel to Identify Selective COX-2 Inhibitors

Abstract

The aim of this work was to study the regulation of LPS-stimulated PGE 2 synthesis by traditional NSAIDs (piroxicam and diclofenac) and a selective COX-2 inhibitor (NS-398), in cultured bovine corneal endothelial cells and retinal pigmentary epithelial cells. The IC50 values of piroxicam and diclofenac were compared with IC50 values of NS-398, diclofenac, in both types of cells, showed higher potency than piroxicam. Diclofenac seemed to be a COX-2 inhibitor because its IC50 values were similar to the IC50 values of NS-398. We suggest that this in vitro cell assay system could be useful for identifying compounds that selectively inhibit COX-2 in ocular tissues.

Ocular Penetration and Anti-inflammatory Activity of Ketorolac 0.45% and Bromfenac 0.09% Against Lipopolysaccharide-Induced Inflammation

“…24 While COX-1 has often been termed the constitutive isoform and COX-2 has been referred to as the inducible isoform, 25,26 these strict definitions may be blurred. In a recent study evaluating the ocular inflammatory response 2 h after paracentesis, inhibition of prostaglandins was achieved by COX-1 selective inhibitors, but not by nimesulide, a COX-2-selective inhibitor.…”

Rapid determination of nimesulide in rabbit aqueous humor by liquid chromatography

“…Tissue injury is associated with the release of numerous inflammatory mediators including prostaglandins that are synthesized from arachidonic acid via endoperoxide biosynthetic pathway, the initial step of which is catalyzed by the enzyme cyclooxygenase. COX-2 is the major form of the isozyme associated with inflammation and the expression of COX-2 is up-regulated in response to inflammatory stimuli in many tissues and, among the others, in ocular tissues [2,3]. Therefore, a rapid and sensitive analytic method for nimesulide could be useful for ocular pharmacokinetic studies.…”