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Updated: Feb 15, 2026

An Alkali-burn Injury Model of Corneal Neovascularization in the Mouse
Published on: April 7, 2014
Topical Timolol Inhibits Corneal Neovascularization in Rabbits
Ali Kasiri1, Mehdi Reza Ghomi1, Mostafa Feghhi1
1Department of Ophthalmology, Ophthalmology Research Center, Jundishapur University of Medical Sciences, Ahvaz, Iran.
Abstract:
Timolol is a non-selective beta-adrenergic antagonist that is similar to propranolol. The mechanism through which these drugs act on the regression of neovascularization is largely unknown. However, it is thought that the drugs may act through vascular endothelial growth factor signaling, vasoconstriction, and vascular endothelial cell apoptosis. The aim of this study was to determine the effect of timolol on corneal neovascularization in rabbits. Neovascularization was induced in the eyes of 20 rabbits. Next, the rabbits were divided into two groups: the timolol (experimental) group received eye drops containing timolol 0.5% twice per day; and the saline (control) group received saline drops twice per day for two weeks. After 7 days, the mean area of corneal neovascularization (presented as a percentage relative to baseline) was significantly lower in the timolol group than in the saline group (4.63 ± 4.61% versus 58.39 ± 6.31%, P < 0.001). After 2 weeks, the mean area of corneal neovascularization was 0.85 ± 1.33% in the timolol group and 1.73 ± 2.06% in the saline group (P = 0.315). After the first week of treatment, timolol significantly reduced the area of neovascularization compared to control. Timolol may increase the rate of recovery from corneal neovascularization.
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