NDLI: Anti-angiogenic effect of luteolin on retinal neovascularization via blockade of reactive oxygen species production.

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Anti-angiogenic effect of luteolin on retinal neovascularization via blockade of reactive oxygen species production.

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Anti-angiogenic effect of luteolin on retinal neovascularization via blockade of reactive oxygen species production.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Yu, Young Suk Kim, Jeong Hun Kim, Jin Hyoung Ryu, Nam Hee Cho, Chang Sik Jun, Hyoung Oh Park, Sung Wook Kim, Jin Sook
Description	Author Affiliation: Park SW ( Fight against Angiogenesis-Related Blindness Laboratory, Clinical Research Institute, Seoul National University Hospital, Seoul, Korea.)
Abstract	PURPOSE: Oxidative stress-induced vascular endothelial growth factor (VEGF) is thought to play a critical role in the pathogenesis of retinopathy of prematurity (ROP). This study was performed to investigate the anti-angiogenic effect of luteolin against reactive oxygen species (ROS)-induced retinal neovascularization. METHODS: The toxicity of luteolin was evaluated through modified 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay in human retinal microvascular endothelial cells (HRMECs) as well as TUNEL staining in the retina of C57BL/6J mice. After intravitreal injection of luteolin in the mouse model of ROP, retinal neovascularization was examined by fluorescence angiography and vessel counting. Anti-angiogenic activity of luteolin was evaluated by VEGF-induced migration and tube formation assay. The effect of luteolin on tertiary-butylhydroperoxide (t-BH)-induced ROS production was measured with 2'7'-dichlorofluorescein diacetate. The effect of luteolin on t-BH-induced and hypoxia-induced VEGF transcription and expression were evaluated by RT-PCR and Western blot, respectively. RESULTS: Luteolin never affected the viability of HRMECs up to 10 µM, where luteolin never induced any structural change in all retinal layers. Luteolin inhibited retinal neovascularization in the mouse model of ROP. Moreover, VEGF-induced migration and tube formation were significantly decreased by cotreatment of luteolin. Luteolin attenuated VEGF transcription via blockade of t-BH-induced ROS production. Luteolin suppressed hypoxia-induced VEGF expression via attenuating hypoxia inducible factor 1 expression. CONCLUSIONS: Our results suggest that luteolin could be a potent anti-angiogenic agent for retinal neovascularization, which is related to anti-oxidative activity to block ROS production and to subsequently suppress VEGF expression and the pro-angiogenic effect of VEGF.
ISSN	01460404
e-ISSN	15525783
Journal	Investigative Opthalmology & Visual Science
Issue Number	12
Volume Number	53
Language	English
Publisher	Association for Research in Vision and Ophthalmology
Publisher Date	2012-11-19
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Down-regulation Luteolin Therapeutic Use Rna, Messenger Reactive Oxygen Species Antagonists & Inhibitors Retina Pathology Retinal Neovascularization Drug Therapy Vascular Endothelial Growth Factor A Genetics Animals Apoptosis Blotting, Western Cell Survival Cells, Cultured Disease Models, Animal Fluorescein Angiography Fundus Oculi In Situ Nick-end Labeling Mice Mice, Inbred Balb C Mice, Inbred C57bl Oxidative Stress Biosynthesis Metabolism Drug Effects Comparative Study Research Support, Non-u.s. Gov't Discipline Ophthalmology
Content Type	Text
Resource Type	Article
Subject	Ophthalmology Sensory Systems Cellular and Molecular Neuroscience

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