Macular pigment lutein is antiinflammatory in preventing choroidal neovascularization
| Autor: | Shigeaki Ohno, Shingo Satofuka, Norihiro Nagai, Kazuhiro Ohgami, Kazuo Tsubota, Yoko Ozawa, Kazuo Umezawa, Kanako Izumi-Nagai, Yuichi Oike, Susumu Ishida |
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| Rok vydání: | 2007 |
| Předmět: |
Male
Vascular Endothelial Growth Factor A Lutein medicine.medical_specialty genetic structures Active Transport Cell Nucleus Anti-Inflammatory Agents Administration Oral Inflammation Angiogenesis Inhibitors Pharmacology Pathogenesis chemistry.chemical_compound Mice NF-KappaB Inhibitor alpha In vivo medicine Animals Chemokine CCL2 Laser Coagulation Dose-Response Relationship Drug business.industry Choroid Monocyte Macrophages Transcription Factor RelA Reproducibility of Results Macular degeneration medicine.disease Intercellular Adhesion Molecule-1 eye diseases Choroidal Neovascularization Surgery Vascular endothelial growth factor Mice Inbred C57BL Disease Models Animal medicine.anatomical_structure Choroidal neovascularization chemistry I-kappa B Proteins sense organs medicine.symptom Cardiology and Cardiovascular Medicine business |
| Zdroj: | Arteriosclerosis, thrombosis, and vascular biology. 27(12) |
| ISSN: | 1524-4636 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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