Sara Moghaddam-Taaheri1, Monica Agarwal2, Juan Amaral1, Irina Fedorova3, Elvira Agrón4, Norman Salem3, Emily Chew4, S Patricia Becerra1. 1. Section of Protein Structure and Function, Laboratory of Retinal Cell and Molecular Biology, USA. 2. Section of Protein Structure and Function, Laboratory of Retinal Cell and Molecular Biology, USA ; Division of Epidemiology and Clinical Applications, National Eye Institute, NIH, USA. 3. National Institute of Alcohol Abuse and Alcoholism, NIH, USA. 4. Division of Epidemiology and Clinical Applications, National Eye Institute, NIH, USA.
Abstract
BACKGROUND: The purpose of this study is to evaluate the effects of docosahexaenoic acid (DHA), a major omega-3-polyunsaturated fatty acid (ω-3-PUFAs), in the development of experimental choroidal neovascularization (CNV) in rodents. METHODS: Experimental second generation Long Evans rats fed with diets of varying ω-3-PUFA content designed to produce significantly different retinal DHA levels were used in our studies. A transgenic mouse model (fat-1) engineered to over-produce DHA was also studied. CNV was induced by rupture of Bruch's membrane using laser photocoagulation. At 7 days after induction, animals were euthanatized, and eyes were collected. RPE/choroid flatmounts were labeled with isolectin IB4 to determine CNV lesion volumes using confocal microscopy and high-performance 3D imaging software. RESULTS: The median of CNV complex volumes of animals with DHA-adequate diets was lower by 63% relative to that of animals with DHA-deficient diets. The median of CNV complex volumes in fat-1 transgenic mice was decreased by 59% relative to that of wild type controls. CONCLUSIONS: Dietary intake or genetic manipulation to increase the sources of DHA significantly diminished the volume of induced CNV lesions in rodents. They suggest that consumption of ω-3-PUFAs may serve to prevent CNV.
BACKGROUND: The purpose of this study is to evaluate the effects of docosahexaenoic acid (DHA), a major omega-3-polyunsaturated fatty acid (ω-3-PUFAs), in the development of experimental choroidal neovascularization (CNV) in rodents. METHODS: Experimental second generation Long Evans rats fed with diets of varying ω-3-PUFA content designed to produce significantly different retinal DHA levels were used in our studies. A transgenicmouse model (fat-1) engineered to over-produce DHA was also studied. CNV was induced by rupture of Bruch's membrane using laser photocoagulation. At 7 days after induction, animals were euthanatized, and eyes were collected. RPE/choroid flatmounts were labeled with isolectin IB4 to determine CNV lesion volumes using confocal microscopy and high-performance 3D imaging software. RESULTS: The median of CNV complex volumes of animals with DHA-adequate diets was lower by 63% relative to that of animals with DHA-deficient diets. The median of CNV complex volumes in fat-1transgenic mice was decreased by 59% relative to that of wild type controls. CONCLUSIONS: Dietary intake or genetic manipulation to increase the sources of DHA significantly diminished the volume of induced CNV lesions in rodents. They suggest that consumption of ω-3-PUFAs may serve to prevent CNV.
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