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Published Online First: 25 October 2007. doi:10.1136/bjo.2007.125179
British Journal of Ophthalmology 2008;92:120-125
Copyright © 2008 by the BMJ Publishing Group Ltd.

ORIGINAL ARTICLES

Effects of an ophthalmic formulation of meloxicam on COX-2 expression, PGE2 release, and cytokine expression in a model of acute ocular inflammation

R Cruz1, J D Quintana-Hau2, J R González2, R Tornero-Montaño2, L M Baiza-Durán2 and L Vega1

1 Sección Externa de Toxicología, CINVESTAV, San Pedro Zacatenco, Mexico
2 Dirección Científica, Laboratorios Sophia SA de CV, Jalisco, Mexico

Correspondence to:
L Vega, Sección Externa de Toxicología, CINVESTAV, Av. IPN 2508, San Pedro Zacatenco, Mexico DF, 07360, Mexico; lvega{at}cinvestav.mx

Aim: To determine the efficacy of meloxicam ophthalmic formulation on COX-2 activity and expression, inflammation-related cytokines expression and inflammation in an ocular inflammation model.

Methods: Ocular inflammation was induced in New Zealand rabbits by topical application of croton oil (3%) for 3 h. An ophthalmic solution of 0.03% meloxicam, 0.1% sodium diclofenac or vehicle (SophisenTM) was administered every 4 h. Conjunctiva, cornea, aqueous humour and vitreous humour were collected.

Results: In irritated eyes, 72 h of meloxicam treatment downregulated COX-2 expression and activity (mRNA by RT-PCR and PGE2 levels by ELISA, respectively) in a time-dependent manner and reduced inflammation. Meanwhile, diclofenac failed to reduce COX-2 mRNA or PGE2 to basal levels after 7 days of treatment. Meloxicam treatment downregulated IL-6 and IFN-{gamma} expression in the conjunctiva and IL-1β and TNF-{alpha} expression in the cornea. Diclofenac failed to modify these cytokines in both tissues. Meloxicam treatment increased the expression of IL-6 in conjunctiva, and IL-10 in cornea, while diclofenac had no effect on these cytokines.

Conclusion: Meloxicam treatment was more efficient than diclofenac in downregulating the expression and activity of COX-2, reducing inflammation, and modifying the inflammatory-related cytokines.

Funding: This project was financed by Laboratorios SOPHIA SA de CV, Mexico.

Competing interests: None declared.


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