title: Inhibitory effect of triamcinolone acetonide on corneal neovascularization.
abstract: BACKGROUND
  Corneal neovascularization (NV) plays an important role in the pathogenesis of corneal disorders. Recently, triamcinolone acetonide (TA) has been reported as a potential treatment for ocular angiogenesis. However, there are no reports on the inhibitory effect of TA on the corneal NV.
  
  
  METHODS
  Triamcinolone acetonide (2 mg) was administered to four rabbits' eyes by a subconjunctival injection immediately after a basic fibroblast growth factor (bFGF)-pellet was placed into the cornea. As a control, four eyes received an injection of distilled water. Four weeks later, the inhibition of corneal NV was evaluated as the percentage ratio of the vessel invasion area to the area that was sandwiched between the pellet and the limbus cornea. To identify the characteristic appearance of new corneal vessels, the control cornea was examined by using the antibody of vascular endothelial growth factor (VEGF). To confirm TA concentration in TA-treated corneas, the TA level was measured using high-performance liquid chromatography.
  
  
  RESULTS
  Neovascularization from the limbus to the pellet was detected in control eyes 4 weeks after the bFGF pellet implantation. TA-treated eyes demonstrated the inhibition of the neovascular response to the pellet. The severity of NV as compared between control and TA-treated eyes was statistically significant (P<0.05). Morphologically, new vessel growth was shown in the control cornea, and endothelial cells of new vessels were positively stained with the antibody of VEGF. TA concentration in TA-treated corneas at 2 weeks showed 63.5+/-42.8 microg/g (n=4, mean +/- SD), while TA was not detected in control and TA-treated corneas at 4 weeks. The level of TA was effectively maintained for at least 2 weeks after the subconjunctival injection.
  
  
  CONCLUSIONS
  We have demonstrated that subconjunctival TA administration inhibited rabbit corneal NV. This agent may prove useful in the treatment of corneal angiogenic disorders.
authors.affiliation: Mitake Eye Clinic, 4-45-19 Aoyama, Morioka City, 020-0133, Japan. mitake@eins.rnac.ne.jp
authors.forename: Masatoshi
authors.initials: M
authors.lastname: Murata
authors.forename: Shinji
authors.initials: S
authors.lastname: Shimizu
authors.forename: Saburo
authors.initials: S
authors.lastname: Horiuchi
authors.forename: Masayuki
authors.initials: M
authors.lastname: Taira
mesh_terms: D000818:Animals; D003228:Conjunctiva; D016510:Corneal Neovascularization / Q000139:chemically induced / Q000473:pathology / Q000517:prevention & control*; D004343:Drug Implants; D016222:Fibroblast Growth Factor 2; D005938:Glucocorticoids / Q000008:administration & dosage*; D007267:Injections; D016850:Limbus Corneae / Q000098:blood supply* / Q000473:pathology; D011817:Rabbits; D014222:Triamcinolone Acetonide / Q000008:administration & dosage*
chemical_list: D004343:Drug Implants; D005938:Glucocorticoids; D016222:Fibroblast Growth Factor 2; D014222:Triamcinolone Acetonide