10 results on '"Naruomi Yamada"'
Search Results
2. [Untitled]
- Author
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Naruomi YAMADA, Hiroshi KANO, and Yukio ASAMI
- Published
- 2016
- Full Text
- View/download PDF
3. Effect of Sesame Lignans on TNF-α-Induced Expression of Adhesion Molecules in Endothelial Cells
- Author
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Yoshikazu Tsuchie, Toshihiko Osawa, Naruomi Yamada, Yoshiaki Miyake, and Mika Mochizuki
- Subjects
Transcription, Genetic ,Endothelium ,Anti-Inflammatory Agents ,Catechols ,Inflammation ,Biology ,Cardiovascular System ,Applied Microbiology and Biotechnology ,Biochemistry ,Lignans ,Umbilical vein ,Cell Line ,Sesamum ,Analytical Chemistry ,chemistry.chemical_compound ,medicine ,Animals ,Humans ,Molecular Biology ,Lignan ,Tumor Necrosis Factor-alpha ,Cell adhesion molecule ,Organic Chemistry ,Endothelial Cells ,General Medicine ,Cell biology ,Endothelial stem cell ,medicine.anatomical_structure ,Gene Expression Regulation ,chemistry ,Cell culture ,Tumor necrosis factor alpha ,medicine.symptom ,Cell Adhesion Molecules ,Biotechnology - Abstract
The expression of cell adhesion molecules (CAMs) has been implicated as one of the most important causes of the development of inflammatory diseases such as atherosclerosis, and, it is speculated that the prevention of it is an effective approach to the control of atherosclerosis. In the present study, we investigated the effect of sesame lignans on the expression of CAMs in human umbilical vein endothelial cells (HUVECs) induced by tumor necrosis factor-alpha (TNF-alpha). Based on cell-ELISA analysis, we found that sesaminol-6-catechol downregulated the TNF-alpha-induced expression of CAMs in a dose-dependent manner. Moreover, these inhibitory effects were caused to be drastically exerted by downregulating the CAM proteins in TNF-alpha-activated HUVECs at transcriptional level. This suggests, that sesaminol-6-catehcol suppresses the expression of CAMs, and may be an active component of sesame lignans.
- Published
- 2010
- Full Text
- View/download PDF
4. Formation of Dopamine Adducts Derived from Brain Polyunsaturated Fatty Acids
- Author
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Toshihiko Osawa, Xuebo Liu, Naruomi Yamada, and Wakako Maruyama
- Subjects
chemistry.chemical_classification ,Monoamine transporter ,biology ,Dopaminergic ,Neurodegeneration ,Cell Biology ,medicine.disease ,medicine.disease_cause ,Biochemistry ,chemistry.chemical_compound ,chemistry ,Dopamine ,Docosahexaenoic acid ,biology.protein ,medicine ,Arachidonic acid ,Molecular Biology ,Oxidative stress ,medicine.drug ,Polyunsaturated fatty acid - Abstract
Oxidative stress appears to be directly involved in the pathogenesis of the neurodegeneration of dopaminergic systems in Parkinson disease. In this study, we formed four dopamine modification adducts derived from docosahexaenoic acid (C22:6/ω-3) and arachidonic acid (C18:4/ω-6), which are known as the major polyunsaturated fatty acids in the brain. Upon incubation of dopamine with fatty acid hydroperoxides and an in vivo experiment using rat brain tissue, all four dopamine adducts were detected. Furthermore, hexanoyl dopamine (HED), an arachidonic acid-derived adduct, caused severe cytotoxicity in human dopaminergic neuroblastoma SH-SY5Y cells, whereas the other adducts were only slightly affected. The HED-induced cell death was found to include apoptosis, which also seems to be mediated by reactive oxygen species generation and mitochondrial abnormality. Additionally, the experiments using monoamine transporter inhibitor and mouse embryonic fibroblast NIH-3T3 cells that lack the monoamine transporter indicate that the HED-induced cytotoxicity might specially occur in the neuronal cells. These data suggest that the formation of the docosahexaenoic acid- and arachidonic acid-derived dopamine adducts in vitro and in vivo, and HED, the arachidonic acid-derived dopamine modification adduct, which caused selective cytotoxicity of neuronal cells, may indicate a novel mechanism responsible for the pathogenesis in Parkinson disease.
- Published
- 2008
- Full Text
- View/download PDF
5. Amide-type adduct of dopamine - plausible cause of Parkinson diseases
- Author
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Xuebo, Liu, Naruomi, Yamada, and Toshihiko, Osawa
- Subjects
Neurons ,Oxidative Stress ,Docosahexaenoic Acids ,Dopamine ,Fatty Acids, Unsaturated ,Humans ,Parkinson Disease ,Lipid Peroxidation ,Amides ,Oxidation-Reduction - Abstract
Dopamine is the endogenous neurotransmitter produced by nigral neurons. Dopamine loss can trigger not only prominent secondary morphological changes, but also changes in the density and sensitivity of dopamine receptors; therefore, it is a sign of PD development. The reasons for dopamine loss are attributed to dopamine's molecular instability due to it is a member of catecholamine family, whose catechol structure contributes to high oxidative stress through enzymatic and non-enzymatic oxidation. Oxidative stress in the brain easily leads to the lipid peroxidation reaction due to a high concentration of polyunsaturated fatty acids (PUFA), such as docosahexaenoic acid (DHA, C22:6/ω-3) and arachidonic acid (AA, C18:4/ω-6). Recent studies have shown that lipid hydroperoxides, the primary peroxidative products, could non-specifically react with primary amino groups to form N-acyl-type (amide-linkage) adducts. Therefore, based on the NH2-teminals in dopamine's structure, the aims of this chapter are to describes the possibility that reactive LOOH species derived from DHA/AA lipid peroxidation may modify dopamine to form amide-linkage dopamine adducts, which might be related to etiology of Parkinson's diseases.
- Published
- 2013
6. Amide-Type Adduct of Dopamine – Plausible Cause of Parkinson Diseases
- Author
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Xuebo Liu, Naruomi Yamada, and Toshihiko Osawa
- Subjects
medicine.medical_specialty ,Chemistry ,medicine.disease_cause ,Lipid peroxidation ,chemistry.chemical_compound ,Endocrinology ,Docosahexaenoic acid ,Dopamine receptor ,Dopamine ,Internal medicine ,medicine ,Catecholamine ,lipids (amino acids, peptides, and proteins) ,Arachidonic acid ,Neurotransmitter ,Oxidative stress ,medicine.drug - Abstract
Dopamine is the endogenous neurotransmitter produced by nigral neurons. Dopamine loss can trigger not only prominent secondary morphological changes, but also changes in the density and sensitivity of dopamine receptors; therefore, it is a sign of PD development. The reasons for dopamine loss are attributed to dopamine’s molecular instability due to it is a member of catecholamine family, whose catechol structure contributes to high oxidative stress through enzymatic and non-enzymatic oxidation. Oxidative stress in the brain easily leads to the lipid peroxidation reaction due to a high concentration of polyunsaturated fatty acids (PUFA), such as docosahexaenoic acid (DHA, C22:6/ω-3) and arachidonic acid (AA, C18:4/ω-6). Recent studies have shown that lipid hydroperoxides, the primary peroxidative products, could non-specifically react with primary amino groups to form N-acyl-type (amide-linkage) adducts. Therefore, based on the NH2-teminals in dopamine’s structure, the aims of this chapter are to describes the possibility that reactive LOOH species derived from DHA/AA lipid peroxidation may modify dopamine to form amide-linkage dopamine adducts, which might be related to etiology of Parkinson’s diseases.
- Published
- 2013
- Full Text
- View/download PDF
7. Assessing the neuroprotective effect of antioxidant food factors by application of lipid-derived dopamine modification adducts
- Author
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Xuebo, Liu, Naruomi, Yamada, and Toshihiko, Osawa
- Subjects
Curcumin ,Cell Survival ,Dopamine ,Tocotrienols ,Tocopherols ,Parkinson Disease ,Dioxoles ,Xanthophylls ,Antioxidants ,Lignans ,Neuroblastoma ,Tandem Mass Spectrometry ,Cell Line, Tumor ,Humans ,Chromatography, High Pressure Liquid - Abstract
Advances in understanding the neurodegenerative pathologies are creating new opportunities for the development of neuroprotective therapies, such as antioxidant food factors, lifestyle modification and drugs. However, the biomarker by which the effect of the agent on neurodegeneration is determined is limited. We here address hexanoyl dopamine (HED), one of novel dopamine adducts derived from brain polyunsaturated acid, referring to its in vitro formation, potent toxicity to SH-SY5Y cells, and application to assess the neuroprotective effect of antioxidative food factors. Dopamine is a neurotransmitter, and its deficiency is a characterized feature in Parkinson's disease (PD); thus, HED provides a new insight into the understanding of dopamine biology and pathophysiology of PD and a novel biomarker for the assessment of neuroprotective therapies. We have established an analytical system for the detection of HED and its toxicity to the neuroblstoma cell line, SH-SY5Y cells. Here, we discuss the characteristics of the system and its applications to investigate the neuroprotective effect of several antioxidants that originate from food.
- Published
- 2010
8. Assessing the Neuroprotective Effect of Antioxidant Food Factors by Application of Lipid-Derived Dopamine Modification Adducts
- Author
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Xuebo Liu, Toshihiko Osawa, and Naruomi Yamada
- Subjects
Antioxidant ,medicine.medical_treatment ,Neurodegeneration ,Pharmacology ,medicine.disease ,Neuroprotection ,In vitro ,Biomarker (cell) ,chemistry.chemical_compound ,chemistry ,Dopamine ,Toxicity ,medicine ,Neurotransmitter ,medicine.drug - Abstract
Advances in understanding the neurodegenerative pathologies are creating new opportunities for the development of neuroprotective therapies, such as antioxidant food factors, lifestyle modification and drugs. However, the biomarker by which the effect of the agent on neurodegeneration is determined is limited. We here address hexanoyl dopamine (HED), one of novel dopamine adducts derived from brain polyunsaturated acid, referring to its in vitro formation, potent toxicity to SH-SY5Y cells, and application to assess the neuroprotective effect of antioxidative food factors. Dopamine is a neurotransmitter, and its deficiency is a characterized feature in Parkinson's disease (PD); thus, HED provides a new insight into the understanding of dopamine biology and pathophysiology of PD and a novel biomarker for the assessment of neuroprotective therapies. We have established an analytical system for the detection of HED and its toxicity to the neuroblstoma cell line, SH-SY5Y cells. Here, we discuss the characteristics of the system and its applications to investigate the neuroprotective effect of several antioxidants that originate from food.
- Published
- 2009
- Full Text
- View/download PDF
9. Assessing the neuroprotective effect of antioxidative food factors by application of lipid-derived dopamine modification adducts
- Author
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Xuebo, Liu, Naruomi, Yamada, and Toshihiko, Osawa
- Subjects
Curcumin ,Cell Survival ,Dopamine ,Tocotrienols ,Tocopherols ,Parkinson Disease ,Dioxoles ,Xanthophylls ,Antioxidants ,Lignans ,Oxidative Stress ,Neuroprotective Agents ,Food ,Tandem Mass Spectrometry ,Cell Line, Tumor ,Humans ,Chromatography, High Pressure Liquid - Abstract
Advances in understanding the neurodegenerative pathologies are creating new opportunities for the development of neuroprotective therapies, such as antioxidant food factors, lifestyle modification, and drugs. However, the biomarker by which to determine the effect of the agent on neurodegeneration is limited. We here address hexanoyl dopamine (HED), one of novel dopamine adducts derived from brain polyunsaturated acid, referring to its in vitro formation, potent toxicity to SH-SY5Y cells, and application to assess the neuroprotective effect of antioxidative food factors. Dopamine is a neurotransmitter and its deficiency is a characterized feature in Parkinson's disease (PD), thereby HED represents a new addition to understanding of dopamine biology and pathophysiology of PD and a novel biomarker for the assessment of neuroprotective therapies. We have established an analytical system using for the detection of HED and its toxicity to the neuroblstoma cell line, SH-SY5Y cells. Here, we discuss the characteristics of the system and its applications to investigate the neuroprotective effect of several antioxidants that originate from food.
- Published
- 2009
10. Lactobacillus gasseri PA-3 Uses the Purines IMP, Inosine and Hypoxanthine and Reduces Their Absorption in Rats.
- Author
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Naruomi Yamada, Chizuru Saito-Iwamoto, Marie Nakamura, Misato Soeda, Yoshika Chiba, Hiroshi Kano, and Yukio Asami
- Subjects
LACTOBACILLUS gasseri ,PURINES ,HYPOXANTHINE ,URIC acid ,BLOOD serum analysis ,LABORATORY rats - Abstract
Excessive intake of purine-rich foods elevates serum levels of uric acid. Animal and fish meats contain high amounts of inosine and its related purines, and the reduction of taking those purines is crucial for the improvement of serum uric acid levels. We previously showed that Lactobacillus gasseri PA-3 (PA-3) incorporates adenosine and its related purines and that oral treatment with PA-3 reduced adenosine absorption in rats. This study investigated whether PA-3 also incorporates IMP (inosine 5'-monophosphate), inosine, and hypoxanthine, and whether it reduces their absorption in rats. PA-3 was incubated in vitro with radioisotope (RI)-labeled IMP, inosine, and hypoxanthine, and the incorporation of these compounds by PA-3 was evaluated. In addition, rats were orally administered PA-3 along with RI-labeled inosine 5'-monophosphate, inosine, or hypoxanthine, and the ability of PA-3 to attenuate the absorption of these purines was determined. PA-3 incorporated all three purines and displayed greater proliferation in the presence than in the absence of these purines. Oral administration of PA-3 to rats reduced the absorption of IMP, inosine, and hypoxanthine. These results indicate that PA-3 reduces the absorption of purines contained in foods and it is expected that PA-3 contributes attenuation of the excessive intake of dietary purines. [ABSTRACT FROM AUTHOR]
- Published
- 2017
- Full Text
- View/download PDF
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