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Effects of an Ophthalmic Formulation of Meloxicam on COX-2 Expression, PGE2 Release, and Cytokine Expression in a Model of Acute Ocular Inflammation
  1. Raymundo Cruz,
  2. Juan de Dios Quintana-Hau,
  3. Jaime R González,
  4. Rubén Tornero-Montaño,
  5. Leopoldo M Baiza-Durán,
  6. Libia Vega (libia68{at}
  1. CINVESTAV, Mexico
  2. Laboratorios SOPHIA, Mexico
  3. Laboratorios Sophia, Mexico
  4. Laboratorios SOPHIA, Mexico
  5. Laboratorios SOPHIA, Mexico
  6. CINVESTAV, Mexico


    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) were administered every 4 h. Conjunctiva, cornea, aqueous and vitreous humor were collected.

    Results: In irritated eyes, 72 h of meloxicam treatment down-regulated 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 down-regulated 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 down-regulating the expression and activity of COX-2, reducing inflammation, and modifying the inflammatory-related cytokines.

    • AINES
    • COX-2
    • Ocular inflammation
    • PGE2
    • Proinflammatory cytokines

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