Related Experiment Video
Updated: Aug 21, 2026

A Mouse Model for Laser-induced Choroidal Neovascularization
Published on: December 27, 2015
COX-2-selective inhibitor, etodolac, suppresses choroidal neovascularization in a mice model
Hidenori Takahashi1, Yasuo Yanagi, Yasuhiro Tamaki
1Department of Ophthalmology, University of Tokyo School of Medicine, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan.
Abstract:
Cyclooxygenases (COXs) are involved in choroidal neovascularization (CNV). However, the relative contribution of COX-1 and -2 to CNV has not been determined. In this study, the expression of COX-2 was investigated in CNVs in a murine laser-induced model. Subsequently, we found that experimental CNV expressed COX-2, most remarkably around the highly vascularized lesions. To examine the effect of COX-2 inhibition on CNV, etodolac, a non-steroidal anti-inflammatory drug with a high COX-2 selectivity, was tested on murine CNV model. The results demonstrated that the intensity of fluorescein leakage from the photocoagulated lesions decreased significantly compared to the control eyes following etodolac administration. The area of CNV lesions, as examined using histological sections and choroidal flatmounts at day 7, demonstrated that the average size of the CNV lesions was significantly reduced in the etodolac-treated eyes compared to the control eyes. Together, our results demonstrated that selective COX-2 inhibition suppresses CNV.
Insights
Selective inhibition of cyclooxygenase-2 (COX-2) suppresses choroidal neovascularization (CNV). Etodolac, a COX-2 inhibitor, significantly reduced CNV lesion size and leakage in a murine model.
Area of Science:
- Ophthalmology
- Molecular Biology
- Pharmacology
Background:
- Cyclooxygenases (COXs) play a role in choroidal neovascularization (CNV).
- The specific roles of COX-1 and COX-2 in CNV remain unclear.
- Understanding COX involvement is crucial for developing targeted therapies.
Purpose of the Study:
- To investigate the expression of COX-2 in a murine laser-induced CNV model.
- To determine the therapeutic effect of selective COX-2 inhibition on CNV progression.
- To evaluate the impact of etodolac on CNV lesion size and vascular leakage.
Main Methods:
- Murine laser-induced model for experimental choroidal neovascularization.
- Immunohistochemical analysis to detect COX-2 expression in CNV lesions.
- Administration of etodolac, a selective COX-2 inhibitor, to assess its therapeutic efficacy.
- Quantification of CNV lesion area and fluorescein leakage.
Main Results:
- COX-2 expression was significantly upregulated in experimental CNV lesions, particularly around vascular areas.
- Etodolac treatment led to a significant reduction in fluorescein leakage from CNV lesions.
- Histological analysis revealed a significant decrease in the average size of CNV lesions in etodolac-treated eyes.
Conclusions:
- The study demonstrates that COX-2 is expressed in experimental CNV.
- Selective inhibition of COX-2 using etodolac effectively suppresses choroidal neovascularization.
- Targeting COX-2 represents a promising therapeutic strategy for managing CNV.

