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Updated: May 24, 2026
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Published on: April 7, 2014
Inhibition of corneal neovascularization in rats by systemic administration of sorafenib
Jeong Won Seo1, So-Hyang Chung, Jun-Sub Choi
1Department of Ophthalmology, Sahmyook Medical Center, Seoul Adventist Hospital, Seoul, Korea.
Purpose:
To evaluate the effect of orally administered sorafenib on corneal neovascularization in rat models.
Methods:
In male Sprague-Dawley rats, a silver nitrate applicator was placed on the central cornea in both eyes to elicit angiogenesis. Rats were divided into 3 groups, the control group and the 2 sorafenib-treated groups (low dose, 30 mg · kg(-1) · day(-1); high dose, 60 mg · kg(-1) · day(-1)). The area of corneal neovascularization was measured by image analysis. Vascular endothelial growth factor receptor 2 (VEGFR2) messenger RNA expression was measured in rat corneas by reverse transcription-polymerase chain reaction, and the expression of phosphorylated extracellular signal-regulated kinase (ERK) was measured by Western blot analysis 1 week after cauterization.
Results:
The area of corneal neovascularization was significantly reduced by 44% in the 30 mg · kg(-1) · day(-1) group and by 66% in the 60 mg · kg(-1) · day(-1) group, compared with the control group (P = 0.014 and P < 0.0001). Corneal VEGFR2 messenger RNA expression was higher in the control group than in the sorafenib-treated groups. The expression of phosphorylated ERK in rat corneas was suppressed in the sorafenib-treated groups but not in the control group.
Conclusions:
Oral administration of a multikinase inhibitor (sorafenib) significantly reduced the development of experimental corneal neovascularization in a dose-dependent manner. This inhibitory effect is probably related to the suppression of ERK phosphorylation by sorafenib.
Insights
Sorafenib, a multikinase inhibitor, effectively reduced experimental corneal neovascularization in rats. This treatment suppressed vascular endothelial growth factor receptor 2 (VEGFR2) and extracellular signal-regulated kinase (ERK) phosphorylation.
Area of Science:
- Ophthalmology
- Pharmacology
- Molecular Biology
Background:
- Corneal neovascularization (CNV) is a pathological process involving new blood vessel growth in the cornea.
- CNV can lead to vision impairment and is associated with increased vascular endothelial growth factor (VEGF) signaling.
- Targeting VEGF signaling pathways is a potential therapeutic strategy for CNV.
Purpose of the Study:
- To investigate the efficacy of orally administered sorafenib in inhibiting corneal neovascularization in a rat model.
- To assess the impact of sorafenib on key molecular markers involved in angiogenesis, including VEGFR2 and ERK signaling.
Main Methods:
- Corneal neovascularization was induced in Sprague-Dawley rats using silver nitrate cauterization.
- Rats were treated with low-dose (30 mg/kg/day) or high-dose (60 mg/kg/day) sorafenib, or served as controls.
- Corneal neovascularization area was quantified by image analysis.
- Vascular endothelial growth factor receptor 2 (VEGFR2) mRNA and phosphorylated extracellular signal-regulated kinase (p-ERK) expression were analyzed using RT-PCR and Western blot, respectively.
Main Results:
- Sorafenib significantly reduced the area of corneal neovascularization in a dose-dependent manner (44% reduction at low dose, 66% at high dose).
- VEGFR2 mRNA expression was lower in sorafenib-treated groups compared to controls.
- Phosphorylated ERK expression was suppressed in corneas of rats treated with sorafenib.
Conclusions:
- Oral sorafenib effectively inhibits experimental corneal neovascularization in rats.
- The anti-angiogenic effect of sorafenib is likely mediated through the suppression of VEGFR2 and ERK phosphorylation.
- Sorafenib demonstrates potential as a therapeutic agent for conditions involving corneal neovascularization.
