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B. A. Kamppeter, F. vom Hagen, H. Hammes, J. Jonas; Proliferative Retinopathy and Thalidomide - A New Target for an Old Drug?. Invest. Ophthalmol. Vis. Sci. 2007;48(13):3425.
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In recent years Thalidomide experienced a comeback after being banned for many years due to its teratogenicity. Newly discovered functional properties include inhibition of proinflammatory cytokines or antiangiogenic effects due to inhibition of VEGF and bFGF (basic fibroblast growth factor). Aim of this study was to evaluate the effect of intravitreal administered Thalidomide in a retinopathy of prematurity model of the mouse.
13 C57 mice (2 litters) received 150µg Thalidomide in one eye at day 12 of a standardized ROP model. A shame injection was performed in the contralateral eye. At day 17 the animals were sacrified and eyes were enucleated. Histological analysis was performed by counting preretinal neovascularisations and measuring retinal thickness. TUNEL staining was applied for count of apoptotic cells. 2 additional litters (12 mice) were sacrified after 31 days and analyzed the same way.
Eyes treated with 150µg Thalidomide showed significantly fewer neovascularisations (22.7±24.0) compared to sham eyes (60.3±27.2; p=0.02). Retinal thickness was 22.05±3.88µm in Thalidomide treated eyes and 23.39±2.58µm in controls. This was not significant (p=0.20). Apoptotic cell count of the outer nuclear layer was significantly (p=0.01) higher in Thalidomide treated eyes when compared to controls (27.8±13.6 vs. 17.6±8.5).
Intravitreal Thalidomide effectively reduces preretinal neovascularisation in the ROP model of the mouse. Intravitreal Thalidomide does not affect retinal thickness significantly, but showed a slight increased apoptosis in the outer nuclear layer of the retina. So far Thalidomide seems to be an effective drug to treat preretinal neovascularisation.
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