Use of flurbiprofen to inhibit corneal neovascularization.
Following the suggestion that prostaglandins are involved in corneal neovascularization, two inhibitors of prostaglandin formation, prednisolone acetate and flurbiprofen sodium, have been evaluated in two experimental models of corneal neovascularization. The fatty acid cyclooxygenase inhibitor, flurbiprofen, at concentrations of 0.01% and 0.1%, significantly decreased the rate of vessel growth compared with vehicle controls in both silver nitrate cauterization and anterior chamber alloxan models of corneal neovascularization. Prednisolone, at a concentration of 1%, was used as a positive control. It did inhibit neovascularization in the latter model, but was ineffective in the former. It is concluded that 0.1% flurbiprofen is equipotent to 1% prednisolone as an inhibitor of corneal neovascularization. The mechanism is unknown but is likely to be via inhibition of prostaglandin formation and/or inhibition of leukocytic infiltration.
D000818:Animals; D003315:Cornea / Q000098:blood supply*; D003864:Depression, Chemical; D005480:Flurbiprofen / Q000494:pharmacology*; D009389:Neovascularization, Pathologic / Q000187:drug effects*; D011239:Prednisolone / Q000494:pharmacology; D011422:Propionates / Q000494:pharmacology*; D011817:Rabbits
D011422:Propionates; D005480:Flurbiprofen; D011239:Prednisolone