Astaxanthine tegen macula degeneratie*
Uit een Japanse studie, weliswaar met muizen blijkt dat astaxanthine goed werkzaam kan zijn tegen de groei van bloedvaatjes onder het netvlies en andere moleculaire mechanisme, symptomen van de natte versie van
macula degeneratie. Astaxanthine
onderdrukt ook de werking van het ontstekingsmolecuul NF-kappaB.
Inhibition of Choroidal Neovascularization with an Anti-Inflammatory Carotenoid Astaxanthin
Kanako Izumi-Nagai,1,2,3 Norihiro Nagai,1,2,3 Kazuhiro Ohgami,4 Shingo Satofuka,1,2 Yoko Ozawa,1,2 Kazuo Tsubota,2 Shigeaki Ohno,4 Yuichi Oike,1,5 and Susumu Ishida1,2
1From the Laboratory of Retinal Cell Biology and the 2Department of Ophthalmology, Keio University School of Medicine, Tokyo, Japan; the 4Department of Ophthalmology and Visual Sciences, Hokkaido University Graduate School of Medicine, Sapporo, Japan; and the 5Department of Molecular Genetics, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
PURPOSE. Astaxanthin (AST) is a carotenoid found in marine animals and vegetables. The purpose of the present study was to investigate the effect of AST on the development of experimental choroidal neovascularization (CNV) with underlying cellular and molecular mechanisms.
METHODS. Laser photocoagulation was used to induce CNV in C57BL/6J mice. Mice were pretreated with intraperitoneal injections of AST daily for 3 days before photocoagulation, and treatments were continued daily until the end of the study. CNV response was analyzed by volumetric measurements 1 week after laser injury. Retinal pigment epithelium–choroid levels of I B- , intercellular adhesion molecule (ICAM)-1, monocyte chemotactic protein (MCP)-1, interleukin (IL)-6, vascular endothelial growth factor (VEGF), VEGF receptor (VEGFR)-1, and VEGFR-2 were examined by Western blotting or ELISA. AST was applied to capillary endothelial (b-End3) cells, macrophages, and RPE cells to analyze the activation of NF- B and the expression of inflammatory molecules.
RESULTS. The index of CNV volume was significantly suppressed by treatment with AST compared with that in vehicle-treated animals. AST treatment led to significant inhibition of macrophage infiltration into CNV and of the in vivo and in vitro expression of inflammation-related molecules, including VEGF, IL-6, ICAM-1, MCP-1, VEGFR-1, and VEGFR-2. Importantly, AST suppressed the activation of the NF- B pathway, including I B- degradation and p65 nuclear translocation.
CONCLUSIONS. AST treatment, together with inflammatory processes including NF- B activation, subsequent upregulation of inflammatory molecules, and macrophage infiltration, led to significant suppression of CNV development. The present study suggests the possibility of AST supplementation as a therapeutic strategy to suppress CNV associated with AMD.
Investigative Ophthalmology and Visual Science. 2008;49:1679-1685 (Oktober
2008)
