Neuroprotective effects of lutein in the retina

Yoko Ozawa, Mariko Sasaki, Noriko Takahashi, Mamoru Kamoshita, Seiji Miyake, Kazuo Tsubota

研究成果: Article

82 引用 (Scopus)

抄録

Although a large variety of pharmaceutical therapies for treating disease have been developed in recent years, there has been little progress in disease prevention. In particular, the protection of neural tissue is essential, because it is hardly regenerated. The use of nutraceuticals for maintaining the health has been supported by several clinical studies, including cross-sectional and interventional studies for age-related macular disease. However, mechanistic evidence for their effects at the molecular level has been very limited. In this review, we focus on lutein, which is a xanthophyll type of carotenoid. Lutein is not synthesized in mammals, and must be obtained from the diet. It is delivered to the retina, and in humans, it is concentrated in the macula. Here, we describe the neuroprotective effects of lutein and their underlying molecular mechanisms in animal models of vision-threatening diseases, such as innate retinal inflammation, diabetic retinopathy, and light-induced retinal degeneration. In lutein-treated mouse ocular disease models, oxidative stress in the retina is reduced, and its downstream pathological signals are inhibited. Furthermore, degradation of the functional proteins, rhodopsin (a visual substance) and synaptophysin (a synaptic vesicle protein also influenced in other neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease), the depletion of brain-derived neurotrophic factor (BDNF), and DNA damage are prevented by lutein, which preserves visual function. We discuss the possibility of using lutein, an antioxidant, as a neuroprotective treatment for humans.

元の言語English
ページ(範囲)51-56
ページ数6
ジャーナルCurrent Pharmaceutical Design
18
発行部数1
DOI
出版物ステータスPublished - 2012 1

Fingerprint

Lutein
Neuroprotective Agents
Retina
Xanthophylls
Retinal Degeneration
Synaptophysin
Rhodopsin
Eye Diseases
Synaptic Vesicles
Brain-Derived Neurotrophic Factor
Diabetic Retinopathy
Dietary Supplements
Neurodegenerative Diseases
Proteolysis
DNA Damage
Parkinson Disease
Mammals
Alzheimer Disease
Oxidative Stress
Animal Models

ASJC Scopus subject areas

  • Drug Discovery
  • Pharmacology

これを引用

Neuroprotective effects of lutein in the retina. / Ozawa, Yoko; Sasaki, Mariko; Takahashi, Noriko; Kamoshita, Mamoru; Miyake, Seiji; Tsubota, Kazuo.

:: Current Pharmaceutical Design, 巻 18, 番号 1, 01.2012, p. 51-56.

研究成果: Article

Ozawa, Y, Sasaki, M, Takahashi, N, Kamoshita, M, Miyake, S & Tsubota, K 2012, 'Neuroprotective effects of lutein in the retina', Current Pharmaceutical Design, 巻. 18, 番号 1, pp. 51-56. https://doi.org/10.2174/138161212798919101
Ozawa, Yoko ; Sasaki, Mariko ; Takahashi, Noriko ; Kamoshita, Mamoru ; Miyake, Seiji ; Tsubota, Kazuo. / Neuroprotective effects of lutein in the retina. :: Current Pharmaceutical Design. 2012 ; 巻 18, 番号 1. pp. 51-56.
@article{b3786b725ec54e88ae3888423585cfcb,
title = "Neuroprotective effects of lutein in the retina",
abstract = "Although a large variety of pharmaceutical therapies for treating disease have been developed in recent years, there has been little progress in disease prevention. In particular, the protection of neural tissue is essential, because it is hardly regenerated. The use of nutraceuticals for maintaining the health has been supported by several clinical studies, including cross-sectional and interventional studies for age-related macular disease. However, mechanistic evidence for their effects at the molecular level has been very limited. In this review, we focus on lutein, which is a xanthophyll type of carotenoid. Lutein is not synthesized in mammals, and must be obtained from the diet. It is delivered to the retina, and in humans, it is concentrated in the macula. Here, we describe the neuroprotective effects of lutein and their underlying molecular mechanisms in animal models of vision-threatening diseases, such as innate retinal inflammation, diabetic retinopathy, and light-induced retinal degeneration. In lutein-treated mouse ocular disease models, oxidative stress in the retina is reduced, and its downstream pathological signals are inhibited. Furthermore, degradation of the functional proteins, rhodopsin (a visual substance) and synaptophysin (a synaptic vesicle protein also influenced in other neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease), the depletion of brain-derived neurotrophic factor (BDNF), and DNA damage are prevented by lutein, which preserves visual function. We discuss the possibility of using lutein, an antioxidant, as a neuroprotective treatment for humans.",
keywords = "BDNF, DNA damage, Lutein, Neuroprotection, Oxidative stress, Protein degradation, Retina, Synaptophysin, Ubiquitin proteasome system, Visual function",
author = "Yoko Ozawa and Mariko Sasaki and Noriko Takahashi and Mamoru Kamoshita and Seiji Miyake and Kazuo Tsubota",
year = "2012",
month = "1",
doi = "10.2174/138161212798919101",
language = "English",
volume = "18",
pages = "51--56",
journal = "Current Pharmaceutical Design",
issn = "1381-6128",
publisher = "Bentham Science Publishers B.V.",
number = "1",

}

TY - JOUR

T1 - Neuroprotective effects of lutein in the retina

AU - Ozawa, Yoko

AU - Sasaki, Mariko

AU - Takahashi, Noriko

AU - Kamoshita, Mamoru

AU - Miyake, Seiji

AU - Tsubota, Kazuo

PY - 2012/1

Y1 - 2012/1

N2 - Although a large variety of pharmaceutical therapies for treating disease have been developed in recent years, there has been little progress in disease prevention. In particular, the protection of neural tissue is essential, because it is hardly regenerated. The use of nutraceuticals for maintaining the health has been supported by several clinical studies, including cross-sectional and interventional studies for age-related macular disease. However, mechanistic evidence for their effects at the molecular level has been very limited. In this review, we focus on lutein, which is a xanthophyll type of carotenoid. Lutein is not synthesized in mammals, and must be obtained from the diet. It is delivered to the retina, and in humans, it is concentrated in the macula. Here, we describe the neuroprotective effects of lutein and their underlying molecular mechanisms in animal models of vision-threatening diseases, such as innate retinal inflammation, diabetic retinopathy, and light-induced retinal degeneration. In lutein-treated mouse ocular disease models, oxidative stress in the retina is reduced, and its downstream pathological signals are inhibited. Furthermore, degradation of the functional proteins, rhodopsin (a visual substance) and synaptophysin (a synaptic vesicle protein also influenced in other neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease), the depletion of brain-derived neurotrophic factor (BDNF), and DNA damage are prevented by lutein, which preserves visual function. We discuss the possibility of using lutein, an antioxidant, as a neuroprotective treatment for humans.

AB - Although a large variety of pharmaceutical therapies for treating disease have been developed in recent years, there has been little progress in disease prevention. In particular, the protection of neural tissue is essential, because it is hardly regenerated. The use of nutraceuticals for maintaining the health has been supported by several clinical studies, including cross-sectional and interventional studies for age-related macular disease. However, mechanistic evidence for their effects at the molecular level has been very limited. In this review, we focus on lutein, which is a xanthophyll type of carotenoid. Lutein is not synthesized in mammals, and must be obtained from the diet. It is delivered to the retina, and in humans, it is concentrated in the macula. Here, we describe the neuroprotective effects of lutein and their underlying molecular mechanisms in animal models of vision-threatening diseases, such as innate retinal inflammation, diabetic retinopathy, and light-induced retinal degeneration. In lutein-treated mouse ocular disease models, oxidative stress in the retina is reduced, and its downstream pathological signals are inhibited. Furthermore, degradation of the functional proteins, rhodopsin (a visual substance) and synaptophysin (a synaptic vesicle protein also influenced in other neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease), the depletion of brain-derived neurotrophic factor (BDNF), and DNA damage are prevented by lutein, which preserves visual function. We discuss the possibility of using lutein, an antioxidant, as a neuroprotective treatment for humans.

KW - BDNF

KW - DNA damage

KW - Lutein

KW - Neuroprotection

KW - Oxidative stress

KW - Protein degradation

KW - Retina

KW - Synaptophysin

KW - Ubiquitin proteasome system

KW - Visual function

UR - http://www.scopus.com/inward/record.url?scp=84855841572&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84855841572&partnerID=8YFLogxK

U2 - 10.2174/138161212798919101

DO - 10.2174/138161212798919101

M3 - Article

C2 - 22211688

AN - SCOPUS:84855841572

VL - 18

SP - 51

EP - 56

JO - Current Pharmaceutical Design

JF - Current Pharmaceutical Design

SN - 1381-6128

IS - 1

ER -