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Updated: Sep 20, 2025

An Alkali-burn Injury Model of Corneal Neovascularization in the Mouse
Published on: April 7, 2014
Treatment Options for Alkali Burn-Induced Corneal Neovascularization: A Comparative Analysis of Two Tyrosine Kinase
Titas Gladkauskas1,2, Ida Marie Rundgren1, Ileana Cristea1,2,3
1Department of Clinical Medicine, University of Bergen, Bergen, Norway.
Purpose:
To evaluate the efficacy of topical dasatinib and axitinib for treating experimentally induced corneal neovascularization (CNV) in a mouse alkali burn model, and to compare these treatments to established therapies like dexamethasone and bevacizumab.
Methods:
Thirty-six C57BL/6; 129 Sv mice underwent a standardized alkali burn to induce CNV in both eyes by applying a paper disc soaked in 1M NaOH to the cornea for 20 seconds. The mice were randomly assigned to one of 6 treatment groups: saline (0.9% sodium chloride), DMSO (5%), dexamethasone (0.1%), bevacizumab (0.5%), dasatinib (0.5%), or axitinib (0.5%). Treatments were applied topically 3 times daily. After 2 weeks of treatment, the mice were sacrificed. CNV assessments, including corneal neovascularization area (CNA), vessel length index (VLI), and limbus vasculature thickness, were conducted postmortem using corneal flat-mounts stained with a CD31 antibody for immunohistochemistry.
Results:
Dexamethasone proved the most effective in inhibiting alkali burn-induced CNA ( P < 0.0001), with bevacizumab showing comparable efficacy ( P < 0.001). Axitinib also effectively reduced CNA ( P < 0.001) and VLI ( P < 0.01). In contrast, dasatinib did not significantly reduce CNA ( P = 0.74) or VLI ( P = 0.98). All eyes in the dexamethasone group developed cataracts compared with 25%-41.7% in the other groups.
Conclusions:
Axitinib reduced CNA and VLI, although not as effectively as other established treatment modalities, whereas dasatinib did not demonstrate significant effects.
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