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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2007;27:2555.)
© 2007 American Heart Association, Inc.

Vascular Biology

Macular Pigment Lutein Is Antiinflammatory in Preventing Choroidal Neovascularization

Kanako Izumi-Nagai; Norihiro Nagai; Kazuhiro Ohgami; Shingo Satofuka; Yoko Ozawa; Kazuo Tsubota; Kazuo Umezawa; Shigeaki Ohno; Yuichi Oike; Susumu Ishida

From the Laboratory of Retinal Cell Biology (K.I.-N., N.N., S.S., Y.O., Y.O., S.I.), the Department of Ophthalmology (K.I.-N., N.N., S.S., Y.O., K.T., S.I.), Keio University School of Medicine, Tokyo, Japan; the Department of Ophthalmology and Visual Sciences (K.O., S.O.), Hokkaido University Graduate School of Medicine, Sapporo, Japan; the Department of Applied Chemistry (K.U.), Faculty of Science and Technology, Keio University, Yokohama, Japan; and the Department of Molecular Genetics (Y.O.), Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.

Correspondence to Susumu Ishida, MD, PhD, Laboratory of Retinal Cell Biology, Department of Ophthalmology, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan. E-mail ishidasu{at}sc.itc.keio.ac.jp

Background— Choroidal neovascularization (CNV) is a critical pathogenesis in age-related macular degeneration, the most common cause of blindness in the developed countries. The aim of the current study was to investigate the effect of lutein supplementation on the development of the murine model of laser-induced CNV together with underlying molecular mechanisms.

Methods and Results— Mice were orally pretreated with lutein daily from 3 days before laser photocoagulation untill the end of the study. The index of CNV volume was significantly suppressed by the treatment with lutein, compared with vehicle-treated animals. Lutein treatment led to significant inhibition of macrophage infiltration into CNV and of the in vivo and in vitro expression of inflammation-related molecules including vascular endothelial growth factor, monocyte chemotactic protein –1, and intercellular adhesion molecule-1. Importantly, lutein suppressed IB- degradation and nuclear translocation of nuclear factor (NF)-B p65 both in vivo and in vitro. Additionally, the development of CNV was significantly suppressed by inhibiting NF-B p65 nuclear translocation, to the levels seen in the lutein treatment.

Conclusions— Lutein treatment led to significant suppression of CNV development together with inflammatory processes including NF-B activation and subsequent upregulation of inflammatory molecules, providing molecular evidence of potential validity of lutein supplementation as a therapeutic strategy to suppress CNV.

We investigate the effect of lutein on experimental choroidal neovascularization (CNV) and revealed that lutein inhibits CNV development together with inflammatory processes including NF-B activation and subsequent upregulation of inflammatory molecules, providing molecular evidence of potential validity of lutein supplementation as a therapeutic strategy to suppress CNV.

Key Words: choroidal neovascularization • lutein • inflammation • nuclear factor-B • age-related macular degeneration

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