Use of flurbiprofen to inhibit corneal neovascularization
C. A. Cooper, M. V. Bergamini and I. H. Leopold
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.