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Updated: Apr 19, 2026
A Mouse Model for Laser-induced Choroidal Neovascularization
Published on: December 27, 2015
Suppression of choroidal neovascularization by Endostar in rats
Jian Liu1, Panpan Ye1, Zhaoan Su1
1Eye Center, Second Affiliated Hospital, Zhejiang University, Hangzhou, Zhejiang 310009, P.R. China.
Abstract:
Choroidal neovascularization (CNV) is common in various retinal and choroidal diseases, and may result in severe and irreversible loss of vision. Our previous studies suggested that Endostar, a novel recombinant endostatin, is able to inhibit the proliferation and migration of choroid‑retinal endothelial cells. To further evaluate the effect of Endostar on the formation of CNV in vivo, a rat model of laser‑induced CNV was constructed and Endostar or phosphate‑buffered saline treatment was administered intravitreally every other day. Using fluorescein angiography (FA), reduced CNV incidence and leakage grade was observed in the Endostar group. In addition, CNV area and maximal thickness were prominently reduced in the Endostar group measured by choroid flat mounts and sections. Furthermore, vascular endothelial growth factor (VEGF), hypoxia‑inducible factor 1α and chemokine C‑X‑C motif ligand 1 were markedly reduced in the Endostar group as determined by quantitative polymerase chain reaction and downregulation of VEGF was also verified by western blot analysis at the protein level. This study demonstrates that Endostar suppressed CNV in a rat model, which may be largely mediated by the downregulation of VEGF and other angiogenic molecules.
Insights
Endostar effectively suppressed choroidal neovascularization (CNV) in a rat model. This treatment reduced CNV formation and thickness, likely by downregulating vascular endothelial growth factor (VEGF) and other pro-angiogenic factors.
Area of Science:
- Ophthalmology
- Angiogenesis Research
- Retinal Diseases
Background:
- Choroidal neovascularization (CNV) is a major cause of vision loss in retinal diseases.
- Endostar, a recombinant endostatin, has shown potential in inhibiting endothelial cell proliferation and migration.
Purpose of the Study:
- To evaluate the in vivo efficacy of Endostar in suppressing laser-induced choroidal neovascularization (CNV) in a rat model.
- To investigate the molecular mechanisms underlying Endostar's anti-CNV effects.
Main Methods:
- A rat model of laser-induced CNV was established.
- Endostar was administered intravitreally.
- CNV formation, leakage, area, and thickness were assessed using fluorescein angiography, choroid flat mounts, and sections.
- Gene and protein expression of angiogenic factors (VEGF, HIF-1α, CXCL1) were analyzed via qPCR and Western blot.
Main Results:
- Endostar treatment significantly reduced CNV incidence and leakage.
- CNV area and thickness were markedly decreased in the Endostar group.
- Expression of VEGF, hypoxia-inducible factor 1α, and chemokine C-X-C motif ligand 1 was significantly downregulated by Endostar.
Conclusions:
- Endostar demonstrates potent anti-angiogenic effects in a rat model of CNV.
- The therapeutic effect of Endostar is associated with the downregulation of VEGF and other key angiogenic molecules.
- Endostar represents a promising therapeutic agent for treating CNV and preventing vision loss.
