Intravitreal human complement factor H in a rat model of laser-induced choroidal neovascularisation

激光诱发脉络膜新生血管的大鼠模型中的玻璃体内人类补体因子 H

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作者:Sang Jin Kim, Jaeryung Kim, Jinyoung Lee, Sung Yoon Cho, Hee Jung Kang, Ki-Yong Kim, Dong-Kyu Jin

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.

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.

Purpose

To investigate the inhibitory effect of intravitreally administered human complement factor H (CFH) in a rat model of laser-induced choroidal neovascularisation (CNV).

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.

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