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Updated: Aug 15, 2026
A Mouse Model for Corneal Neovascularization by Alkali Burn
Published on: June 30, 2023
Plasminogen kringle 5 inhibits alkali-burn-induced corneal neovascularization
Zhihong Zhang1, Jian-Xing Ma, Guoquan Gao
1Zhongshan Ophthalmic Center, Zhongshan University, Guangzhou, People's Republic of China.
Purpose:
Plasminogen kringle 5 (K5) is a potent angiogenic inhibitor. The purpose of the present study was to evaluate the therapeutic effect of K5 on alkali-burn-induced corneal neovascularization (NV) and to investigate its mechanism of action.
Methods:
Corneal NV was induced in rabbits by NaOH. The rabbits received eye drops containing K5 or vehicle alone, four times per day. Corneal NV and inflammation were monitored every other day with a slit lamp microscope, and the length of the vessels in the cornea and the area of NV were measured. Vascular endothelial growth factor (VEGF) was determined by immunohistochemical and Western blot analyses. The TUNEL assay was used to assess the apoptosis of endothelial cells. The effects of K5 on primary bovine aortic endothelial cells (BAECs) were determined by MTT assay, flow cytometry, transmission electron microscopy, and DNA fragmentation assay.
Results:
Alkali-burn-induced progressive corneal NV and inflammation in the cornea. K5 delayed the onset of corneal NV (P < 0.05) and decreased NV areas (P < 0.05) in a dose-dependent manner. K5 treatment, after the formation of corneal NV, induced regression of newly formatted vessels in the cornea. K5 decreased the inflammatory index in the corneas at different time points after the alkali burn. Corneal VEGF levels were reduced by K5 treatment. K5 inhibits proliferation and induces apoptosis in BAECs.
Conclusions:
Topical application of K5 may have therapeutic potential for the chemical burn-induced corneal NV and inflammation. The inhibitory effect of K5 on corneal NV may be by downregulation of VEGF expression.
Insights
Plasminogen kringle 5 (K5) effectively inhibits corneal neovascularization and inflammation after alkali burns in rabbits. This therapeutic agent shows potential for treating chemical burn-induced eye injuries by reducing vascular endothelial growth factor (VEGF).
Area of Science:
- Ophthalmology
- Angiogenesis research
- Corneal disease
Background:
- Corneal neovascularization (NV) is a significant cause of vision impairment.
- Alkali burns are a common cause of severe corneal injury and subsequent NV.
- Angiogenic inhibitors are being explored for therapeutic applications in ocular diseases.
Purpose of the Study:
- To assess the therapeutic efficacy of plasminogen kringle 5 (K5) in alkali-burn-induced corneal NV in a rabbit model.
- To elucidate the underlying mechanism of K5's action on corneal NV and inflammation.
Main Methods:
- Corneal NV was induced using sodium hydroxide (NaOH) in rabbits.
- Rabbits received topical K5 eye drops, and corneal NV and inflammation were monitored.
- Vascular endothelial growth factor (VEGF) levels, endothelial cell apoptosis, and proliferation were analyzed.
Main Results:
- K5 significantly delayed the onset and reduced the area of corneal NV in a dose-dependent manner.
- K5 treatment promoted the regression of established corneal vessels and decreased inflammation.
- K5 downregulated VEGF expression and inhibited endothelial cell proliferation while inducing apoptosis.
Conclusions:
- Topical K5 demonstrates therapeutic potential for managing alkali burn-induced corneal NV and inflammation.
- The anti-angiogenic effect of K5 is likely mediated through the downregulation of VEGF.
