Format

Send to

Choose Destination
Arterioscler Thromb Vasc Biol. 2007 Dec;27(12):2555-62. Epub 2007 Oct 11.

Macular pigment lutein is antiinflammatory in preventing choroidal neovascularization.

Author information

1
Laboratory of Retinal Cell Biology, Department of Ophthalmology, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan.

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

PMID:
17932319
DOI:
10.1161/ATVBAHA.107.151431
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Atypon
Loading ...
Support Center