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E.-K. Lee, J. Kim, K.-W. Kim, Y. Yu, J. Kim; Anti-Angiogenic Effect of Decursin on Retinal Neovasularization of Oxygn-Induced Retinopathy. Invest. Ophthalmol. Vis. Sci. 2010;51(13):4474.
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This study was undertaken to evaluate the inhibitory effect of decursin on retinal neovascularization.
Anti-angiogenic activity of decursin was evaluated by vascular endothelial growth factor (VEGF)-induced proliferation, migration and in vitro tube formation assay of human retinal microvascular endothelial cells (HRMECs). Also, inhibition of VEGFR-2 phosphorylation by decursin was measured by Western blot analysis. After intravitreal injection of decursin in the mouse model of ROP, retinal neovascularization was examined by fluorescence angiography and vessel counting in cross sections. The toxicity of decursin was evaluated through MTT assay in HRMECs as well as histological examination and immunohistochemistry for glial fibrillary acidic protein in the retina.
Decursin significantly inhibited VEGF-induced proliferation, migration and capillary-like networks formation of retinal endothelial cells in dose-dependent manner. Decursin inhibited VEGF-induced phosphorylation of VEGFR-2 to block VEGFR-2 signaling pathway. When intravitreously injected, decursin dramatically suppressed retinal neovascularization in the mouse model of ROP. Even in a high concentration, decursin never induced any structural change and inflammatory cell in all retinal layers as well as vitreous. Moreover, the up-regulation of GFAP expression was not detected in Mueller cells.
Our data suggests that decursin might be a potent anti-angiogenic agent targeting VEGFR-2 signaling pathway, which significantly inhibits retinal neovascularization without retinal toxicity and be applied to variable vaso-proliferative retinopathies as well.
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