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Published on: August 16, 2014
Anti-angiogenic effect of KR-31831 on corneal and choroidal neovascularization in rat models
In-Tae Kim1, Hae-Young Lopilly Park, Jun-Sub Choi
1Kim and Kim Eye Clinic, Seoul, Korea.
Purpose:
We attempt to determine the effect and mechanism of KR-31831 in rat models of corneal neovascularization and choroidal neovascularization (CNV).
Methods:
Corneal neovascularization was induced by silver nitrate cauterization. Balanced salt solution (for control), KR-31831 (0.1 mg/mL), and bevacizumab (10 mg/mL) were applied topically with or without subsequent subconjunctival injection (10 μL). The degree of corneal neovascularization was compared among treatments. The effects of intravitreal (0.1 and 0.3 mg/mL) and intraperitoneal (25 mg/kg) of KR-31831, and intravitreal injection of bevacizumab (2.5 mg/mL) were compared in a laser-induced CNV model. FITC-dextran was used to observe the choroid vessels and to evaluate vessel leakage by fluorescence intensity.
Results:
In the silver nitrate cauterized rat, topical KR-31831 (P = 0.008) or bevacizumab (P = 0.008) reduced effectively the area of corneal neovascularization compared to control on day 14. This was reduced further by additional subconjunctival injection of KR-31831 (P = 0.024) and bevacizumab (P = 0.016). After KR-31831 application, vascular endothelial growth factor (VEGF) receptor 2 and matrix metalloproteinase (MMP)-2 expression was decreased in the cornea. In the CNV model, intravitreal (0.3 mg/mL) and intraperitoneal KR-31831 inhibited significantly the CNV area (P = 0.008 and P = 0.008, respectively) and fluorescence leakage (P = 0.008 and P = 0.032, respectively). This effect was more significant compared to intravitreal bevacizumab in terms of the CNV area (P = 0.032 and P = 0.008, respectively) and fluorescence leakage (P = 0.016 and P = 0.008, respectively).
Conclusions:
The anti-angiogenic effect of KR-31831 was comparable in the cornea and more effective in the choroid compared to that of bevacizumab, and it may exert its effect by VEGF signaling and MMP-2.
Insights
KR-31831 demonstrates potent anti-angiogenic effects in rat models, comparable to bevacizumab in corneal neovascularization and superior in choroidal neovascularization (CNV). Its mechanism involves downregulating VEGF signaling and MMP-2.
Area of Science:
- Ophthalmology
- Angiogenesis Research
- Pharmacology
Background:
- Neovascularization, the formation of new blood vessels, is implicated in various ocular diseases.
- Corneal neovascularization and choroidal neovascularization (CNV) significantly impair vision.
- Developing effective anti-angiogenic therapies is crucial for treating these conditions.
Purpose of the Study:
- To evaluate the efficacy and mechanism of KR-31831 in rat models of corneal neovascularization and CNV.
- To compare the anti-angiogenic potential of KR-31831 with bevacizumab.
Main Methods:
- Corneal neovascularization was induced using silver nitrate cauterization in rats.
- Topical and subconjunctival applications of KR-31831 and bevacizumab were compared.
- Laser-induced CNV model was used to assess intravitreal and intraperitoneal administration of KR-31831.
- FITC-dextran was employed to quantify vascular leakage and observe choroidal vessels.
Main Results:
- Both KR-31831 and bevacizumab significantly reduced corneal neovascularization.
- KR-31831 demonstrated superior inhibition of CNV area and vascular leakage compared to bevacizumab.
- KR-31831 application led to decreased expression of VEGF receptor 2 and MMP-2 in corneal tissues.
Conclusions:
- KR-31831 exhibits significant anti-angiogenic properties in ocular models.
- Its efficacy in treating CNV is more pronounced than that of bevacizumab.
- The therapeutic effect of KR-31831 is likely mediated through the VEGF signaling pathway and MMP-2 inhibition.
