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Updated: May 15, 2026
A Mouse Model for Laser-induced Choroidal Neovascularization
Published on: December 27, 2015
Intravitreal human complement factor H in a rat model of laser-induced choroidal neovascularisation
Sang Jin Kim1, Jaeryung Kim, Jinyoung Lee
1Department of Ophthalmology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea.
Purpose:
To investigate the inhibitory effect of intravitreally administered human complement factor H (CFH) in a rat model of laser-induced choroidal neovascularisation (CNV).
Methods:
Analysis of alternative pathway inhibition by human plasma-purified CFH was conducted by measuring C3 deposition on zymosan particles using rat serum. CNV was induced by laser photocoagulation on Day 0 in the eyes of Brown Norway rats. Human plasma-purified CFH (50 μg/2 μl) or phosphate buffered saline was injected intravitreally on Day 0 (prevention arm) or Day 7 (treatment arm). Seven days after injection, eyes were enucleated and retinal pigment epithelium-choroid-sclera flat mounts were prepared. Areas of CNV were determined in flat mounts and quantified using an image analysis programme. Flat mounts were also stained for membrane attack complex.
Results:
In rat serum, human CFH inhibited activity of alternative pathway in a dose-dependent manner. On Day 3, mean membrane attack complex deposition in laser-treated retina significantly decreased in CFH-treated eyes (p<0.001). In the prevention arm, the mean CNV area in CFH-treated eyes decreased by 27.0% compared with phosphate buffered saline-treated control eyes on Day 7 (p=0.011). In the treatment arm, the mean CNV area in CFH-treated eyes decreased by 38.3% compared with control eyes on Day 14 (p=0.001).
Conclusions:
Intravitreal injection of human CFH resulted in the suppression of formation of new, and regression of preformed laser-induced CNV in the rat model. Human CFH may be a feasible treatment for CNV associated with age-related macular degeneration or other causes.
