Br J Ophthalmol 92:120-125 doi:10.1136/bjo.2007.125179
  • Original Article
    • Laboratory science

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

Open Access
  1. R Cruz1,
  2. J D Quintana-Hau2,
  3. J R González2,
  4. R Tornero-Montaño2,
  5. L M Baiza-Durán2,
  6. L Vega1
  1. 1
    Sección Externa de Toxicología, CINVESTAV, San Pedro Zacatenco, Mexico
  2. 2
    Dirección Científica, Laboratorios Sophia SA de CV, Jalisco, Mexico
  1. L Vega, Sección Externa de Toxicología, CINVESTAV, Av. IPN 2508, San Pedro Zacatenco, Mexico DF, 07360, Mexico; lvega{at}
  • Accepted 29 June 2007
  • Published Online First 25 October 2007


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 (Sophisen™) 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-γ expression in the conjunctiva and IL-1β and TNF-α 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.

Open Access

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