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Y. S. Yu, J. Kim, J. Kim, H.-Y. Lee, K.-W. Kim; Deguelin Inhibits Retinal Neovascularization by Down-Regulation of HIF-1 in Oxygen-Induced Retinopathy. Invest. Ophthalmol. Vis. Sci. 2008;49(13):2632.
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© ARVO (1962-2015); The Authors (2016-present)
To evaluate the anti-angiogenic effect of deguelin on retinal neovascularization
In mice model of oxygen-induced retinopathy with or without intravitreal deguelin, neovascularization was measured through flourescein angiography using FITC-dextran and blood vessel count in cross section. Transcriptional activity and protein expression of hypoxia inducible factor (HIF)-1α was investigated with treatment of deguelin. To determine inhibitory activity for endothelial cell proliferation of deguelin, MTT assay was performed. In addition, deguelin-induced retinal toxicity was evaluated as well.
Deguelin significantly reduces retinal neovascularization in a mouse model of ROP. Deguelin never affected the transcriptional activity of hypoxia inducible factor (HIF)-1α, however, reduced HIF-1α expression, which led to the decrease of vascular endothelial growth factor expression. Deguelin effectively suppressed endothelial cell proliferation without cytotoxic effect under therapeutic concentration range. In addition, deguelin demonstrated no reduction or retardation in normal retinal development and no retinal toxicity.
Our data suggests that deguelin is a potent inhibitor of retinal neovascularization and may be applied in the treatment of other vasoproliferative retinopathies.
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