Macular pigment lutein is antiinflammatory in preventing Choroidal neovascularization
Macular pigment lutein is antiinflammatory in preventing Choroidal neovascularization
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DOI：
10.1161/atvbaha.107.151431
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发表时间：
2007-12-01
影响因子：
8.7
通讯作者：
Ishida, Susumu
中科院分区：
文献类型：
--
作者：
Izumi-Nagai, Kanako;Nagai, Norihiro;Ishida, Susumu
背景-脉络膜新生血管（CNV）是年龄相关性黄斑变性的重要发病机制，年龄相关性黄斑变性是发达国家最常见的致盲原因。本研究的目的是探讨叶黄素补充对激光诱导CNV.Methods和结果小鼠模型的发展与潜在的分子mechanism.Methods和结果的影响，小鼠口服预处理叶黄素，每天从激光光凝前3天，直到研究结束。与溶剂处理的动物相比，叶黄素处理显著抑制CNV体积指数。叶黄素治疗导致显着抑制巨噬细胞浸润到CNV和炎症相关分子，包括血管内皮生长因子，单核细胞趋化蛋白-1，1和细胞间粘附分子-1的体内和体外表达。重要的是，叶黄素抑制I κ B-α降解和核因子（NF）-κ Bp 65的核转位在体内和体外。此外，通过抑制NF-κ B p65核转位，CNV的发展被显著抑制到叶黄素治疗中所见的水平。结论-叶黄素治疗导致CNV发展以及炎症过程的显著抑制，包括NF-κ B激活和随后的炎症分子上调，提供叶黄素补充作为抑制CNV的治疗策略的潜在有效性的分子证据。
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 I kappa B-alpha degradation and nuclear translocation of nuclear factor (NF)-kappa Bp65 both in vivo and in vitro. Additionally, the development of CNV was significantly suppressed by inhibiting NF-kappa 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-kappa B activation and subsequent upregulation of inflammatory molecules, providing molecular evidence of potential validity of lutein supplementation as a therapeutic strategy to suppress CNV.