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

Research output: Contribution to journalArticle

104 Citations (Scopus)

Abstract

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 IκB-α degradation and nuclear translocation of nuclear factor (NF)-κB p65 both in vivo and in vitro. Additionally, the development of CNV was significantly suppressed by inhibiting NF-κB 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-κB activation and subsequent upregulation of inflammatory molecules, providing molecular evidence of potential validity of lutein supplementation as a therapeutic strategy to suppress CNV.

Original languageEnglish
Pages (from-to)2555-2562
Number of pages8
JournalArteriosclerosis, Thrombosis, and Vascular Biology
Volume27
Issue number12
DOIs
Publication statusPublished - 2007 Dec

Fingerprint

Lutein
Choroidal Neovascularization
Anti-Inflammatory Agents
Lasers
Therapeutics
Macular Pigment
Light Coagulation
Chemokine CCL2
Macular Degeneration
Intercellular Adhesion Molecule-1
Blindness
Developed Countries
Vascular Endothelial Growth Factor A
Up-Regulation
Macrophages
Inflammation

Keywords

  • Age-related macular degeneration
  • Choroidal neovascularization
  • Inflammation
  • Lutein
  • Nuclear factor-κB

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Macular pigment lutein is antiinflammatory in preventing choroidal neovascularization. / Izumi-Nagai, Kanako; Nagai, Norihiro; Ohgami, Kazuhiro; Satofuka, Shingo; Ozawa, Yoko; Tsubota, Kazuo; Umezawa, Kazuo; Ohno, Shigeaki; Oike, Yuichi; Ishida, Susumu.

In: Arteriosclerosis, Thrombosis, and Vascular Biology, Vol. 27, No. 12, 12.2007, p. 2555-2562.

Research output: Contribution to journalArticle

Izumi-Nagai, Kanako ; Nagai, Norihiro ; Ohgami, Kazuhiro ; Satofuka, Shingo ; Ozawa, Yoko ; Tsubota, Kazuo ; Umezawa, Kazuo ; Ohno, Shigeaki ; Oike, Yuichi ; Ishida, Susumu. / Macular pigment lutein is antiinflammatory in preventing choroidal neovascularization. In: Arteriosclerosis, Thrombosis, and Vascular Biology. 2007 ; Vol. 27, No. 12. pp. 2555-2562.
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abstract = "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 IκB-α degradation and nuclear translocation of nuclear factor (NF)-κB p65 both in vivo and in vitro. Additionally, the development of CNV was significantly suppressed by inhibiting NF-κB 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-κB activation and subsequent upregulation of inflammatory molecules, providing molecular evidence of potential validity of lutein supplementation as a therapeutic strategy to suppress CNV.",
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AU - Satofuka, Shingo

AU - Ozawa, Yoko

AU - Tsubota, Kazuo

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AU - Oike, Yuichi

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AB - 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 IκB-α degradation and nuclear translocation of nuclear factor (NF)-κB p65 both in vivo and in vitro. Additionally, the development of CNV was significantly suppressed by inhibiting NF-κB 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-κB activation and subsequent upregulation of inflammatory molecules, providing molecular evidence of potential validity of lutein supplementation as a therapeutic strategy to suppress CNV.

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