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Neurodegenerative influence of oxidative stress in the retina of a murine model of diabetes

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Title: Neurodegenerative influence of oxidative stress in the retina of a murine model of diabetes
Authors: Sasaki, M. Browse this author
Ozawa, Y. Browse this author
Kurihara, T. Browse this author
Kubota, S. Browse this author
Yuki, K. Browse this author
Noda, K. Browse this author →KAKEN DB
Kobayashi, S. Browse this author
Ishida, S. Browse this author
Tsubota, K. Browse this author
Keywords: Apoptosis
BDNF
Diabetes
ERK
Lutein
Oxidative stress
Retina
ROS
Visual function
Synaptophysin
Issue Date: May-2010
Publisher: Springer Berlin / Heidelberg
Journal Title: Diabetologia
Volume: 53
Issue: 5
Start Page: 971
End Page: 979
Publisher DOI: 10.1007/s00125-009-1655-6
Abstract: Aims/hypothesis: Diabetic retinopathy is a progressive neuro-degenerative disease, but the underlying mechanism is still obscure. Here, we focused on oxidative stress in the retina, and analysed its influence on retinal neurodegeneration, using an antioxidant, lutein. Methods: C57BL/6 mice with streptozotocin-induced diabetes were constantly fed either a lutein-supplemented diet or a control diet from the onset of diabetes, and their metabolic data were recorded. In 1-month-diabetic mice, reactive oxygen species (ROS) in the retina were measured using dihydroethidium and visual function was evaluated by electroretinograms. Levels of activated extracellular signal-regulated kinase (ERK), synaptophysin and brain-derived neurotrophic factor (BDNF) were also measured by immunoblotting in the retina of 1-month-diabetic mice. In the retinal sections of 4-month-diabetic mice, histological changes, cleaved caspase-3 and TUNEL staining were analysed. Results: Lutein did not affect the metabolic status of the diabetic mice, but it prevented ROS generation in the retina and the visual impairment induced by diabetes. ERK activation, the subsequent synaptophysin reduction, and the BDNF depletion in the diabetic retina were all prevented by lutein. Later, in 4-month-diabetic mice, a decrease in the thickness of the inner plexiform and nuclear layers, and ganglion cell number, together with increase in cleaved caspase-3- and TUNEL-positive cells, were avoided in the retina of lutein-fed mice. Conclusions/interpretation: The results indicated that local oxidative stress that has a neurodegenerative influence in the diabetic retina is prevented by constant intake of a lutein-supplemented diet. The antioxidant, lutein may be a potential therapeutic approach to protect visual function in diabetes.
Type: article
URI: http://hdl.handle.net/2115/48560
Appears in Collections:医学院・医学研究院 (Graduate School of Medicine / Faculty of Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 野田 航介

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