Biology, Behavioral Test Scores Could Be Linked to the Protein Expression Values of p62 and GLAST in the Brains of Mice with Neuropsychiatric Disorder-Related Behaviors, Yuka Ikeda; Moeka Nakashima; Sayuri Yoshikawa; Kurumi Taniguchi; Naoko Suga; Satoru Matsuda, Neuropsychiatric disorders are a public health concern, in which diagnosis and prognosis may be based on clinical symptoms that might often diverge across individuals. Schizophrenia is a major neuropsychiatric disorder, which may affect millions worldwide. However, the biochemical alterations of this disorder have not been comprehensively distinguished. In addition, there is less confidence in finding specific biomarkers for neuropsychiatric disorders, including schizophrenia, but rather a specific characteristic behavioral pattern. In general, maternal immune activation is considered to be one of the important factors in the development of neuropsychiatric disorders. Here, a mouse model of neuropsychiatric disorders was created, in which poly I:C, sodium dextran sulfate (DSS), and κ-carrageenan (CGN) were utilized for maternal immune activation during the pregnancies of mother mice. Subsequently, we examined the link between biochemical changes in p62 and/or glutamate aspartate transporter (GLAST) in the brains of offspring mice and the alteration in their experimental behavior scores. Furthermore, a therapeutic study was conducted on these neuropsychiatric disorder model mice using butyric acid, piceid, and metformin. It was found that some molecules could effectively improve the behavioral scores of neuropsychiatric model mice. Importantly, significant correlations between certain behavioral scores and p62 protein expression, as well as between the scores and GLAST expression, were recognized. This is the first report of a significant correlation between pathological behaviors and biochemical alterations in neuropsychiatric disorder model animals. This concept could contribute to the development of innovative treatments to at least ameliorate the symptoms of several psychiatric disorders., Dec. 2024, 13, 12, Scientific journal, 10.3390/biology13121039

Discovery medicine, Exosomes, Endosomes, and Caveolae as Encouraging Targets with Favorable Gut Microbiota for the Innovative Treatment of Alzheimer's Diseases., Moeka Nakashima; Naoko Suga; Akari Fukumoto; Sayuri Yoshikawa; Satoru Matsuda, Neurodegenerative diseases are characterized by progressive damage to specific neuronal cells, resulting in cognitive impairments. Alzheimer's disease is one of the most common types of cognitive impairments. Until recently, strategies that prevent its clinical progression have remained elusive. It has been suggested that oxidative stress, mitochondrial injury, and inflammation might lead to brain cell death in many neurological disorders. Therefore, the identification of effective neuroprotective agents is a research priority, and several autophagy-targeted bioactive compounds are promising candidate therapeutics for the prevention of brain cell damage. Some Alzheimer's disease risk genes expressed within the brain are linked to cholesterol metabolism, lipid transport, endocytosis, exocytosis, and/or caveolae formation, suggesting fruitful therapeutic targets for the treatment of cognitive impairments. Among them, a well-known genetic risk factor for late-onset Alzheimer's disease is allelic variation of the Apolipoprotein E (APOE) genes. APOE proteins may regulate aspects of cellular homeostasis, which is perturbed in the brain in Alzheimer's disease. Interestingly, the Apolipoprotein E ε4 allele (APOE4) protein is related to autophagy and to the biogenesis of caveolae, endosomes, and exosomes, processes which might consequently be involved in the pathogenesis of neurodegenerative diseases, including Alzheimer's disease. Recent research suggests that modification of the diet and/or gut-microbiota could be effective for treatment of various neurodegenerative diseases. Collectively, this research direction has the potential to improve clinical care through disease-modifying treatment strategies with benefits for patients with neurodegenerative diseases., Nov. 2024, 36, 190, 2132, 2142, Scientific journal, True, 10.24976/Discov.Med.202436190.196

Molecules (Basel, Switzerland), Caveolae with GLP-1 and NMDA Receptors as Crossfire Points for the Innovative Treatment of Cognitive Dysfunction Associated with Neurodegenerative Diseases., Moeka Nakashima; Naoko Suga; Sayuri Yoshikawa; Satoru Matsuda, Some neurodegenerative diseases may be characterized by continuing behavioral and cognitive dysfunction that encompasses memory loss and/or apathy. Alzheimer's disease is the most typical type of such neurodegenerative diseases that are characterized by deficits of cognition and alterations of behavior. Despite the huge efforts against Alzheimer's disease, there has yet been no successful treatment for this disease. Interestingly, several possible risk genes for cognitive dysfunction are frequently expressed within brain cells, which may also be linked to cholesterol metabolism, lipid transport, exosomes, and/or caveolae formation, suggesting that caveolae may be a therapeutic target for cognitive dysfunctions. Interestingly, the modulation of autophagy/mitophagy with the alteration of glucagon-like peptide-1 (GLP-1) and N-methyl-d-aspartate (NMDA) receptor signaling may offer a novel approach to preventing and alleviating cognitive dysfunction. A paradigm showing that both GLP-1 and NMDA receptors at caveolae sites may be promising and crucial targets for the treatment of cognitive dysfunctions has been presented here, which may also be able to modify the progression of Alzheimer's disease. This research direction may create the potential to move clinical care toward disease-modifying treatment strategies with maximal benefits for patients without detrimental adverse events for neurodegenerative diseases., 20 Aug. 2024, 29, 16, Scientific journal, True, 10.3390/molecules29163922

Genes, Potential Molecular Mechanisms of Alcohol Use Disorder with Non-Coding RNAs and Gut Microbiota for the Development of Superior Therapeutic Application., Moeka Nakashima; Naoko Suga; Sayuri Yoshikawa; Yuka Ikeda; Satoru Matsuda, Many investigations have evaluated the expression of noncoding RNAs (ncRNAs) as well as their related molecular functions and biological machineries in individuals with alcohol dependence. Alcohol dependence may be one of the most prevailing psychological disorders globally, and its pathogenesis is intricate and inadequately comprehended. There is substantial evidence indicating significant links between multiple genetic factors and the development of alcohol dependence. In particular, the critical roles of ncRNAs have been emphasized in the pathology of mental illnesses, probably including alcohol dependence. In the comprehension of the action of ncRNAs and their machineries of modification, furthermore, they have emerged as therapeutic targets for a variety of psychiatric illnesses, including alcohol dependence. It is worth mentioning that the dysregulated expression of ncRNAs has been regularly detected in individuals with alcohol dependence. An in-depth knowledge of the roles of ncRNAs and m6A modification may be valuable for the development of a novel treatment against alcohol dependence. In general, a more profound understanding of the practical roles of ncRNAs might make important contributions to the precise diagnosis and/or actual management of alcohol dependence. Here, in this review, we mostly focused on up-to-date knowledge regarding alterations and/or modifications in the expression of ncRNAs in individuals with alcohol dependence. Then, we present prospects for future research and therapeutic applications with a novel concept of the engram system., 29 Mar. 2024, 15, 4, Scientific journal, True, 10.3390/genes15040431

Discovery medicine, Recent Progress of Chitosan Nanoparticles for the Development of Superior Delivery of Vaccines., Moeka Nakashima; Naoko Suga; Yuka Ikeda; Sayuri Yoshikawa; Satoru Matsuda, Chitosan seems to be an innovative biological material potentially utilized as a nanoparticle carrier for drug delivery, which could be low toxic, biocompatible, and easy to prepare. Chitosan nanoparticles have been employed in gene delivery. As a type of multifunctional adjuvant, chitosan nanoparticles could activate the phosphoinositide 3-kinase (PI3K)/AKT signaling pathway to induce cell protection and/or proliferation via the modulation of autophagy within dendritic cells. In general, adjuvants may improve the innate and/or adaptive immune responses to a vaccine antigen by facilitating the antigen presentation of antigen presenting cells such as dendritic cells. The choice of a suitable adjuvant has become vital for improved safety and/or expanded application of vaccines. Fortunately, chitosan nanoparticles could be designed to target the dendritic cells to be enhanced by its adjuvant effect and for stimulating robust immune responses. Therefore, chitosan nanoparticles may be a good immune stimulant with encouraging properties for the development of superior vaccine delivery. Indeed, vaccines could play a key role in human health. In this review, we summarize the concept and/or recent progress in the field of chitosan nanoparticles, providing a valuable resource for investigating the molecular mechanisms of chitosan for the development of a greater vaccine., Mar. 2024, 36, 182, 457, 466, Scientific journal, True, 10.24976/Discov.Med.202436182.43

Biomolecules, Inspiring Tactics with the Improvement of Mitophagy and Redox Balance for the Development of Innovative Treatment against Polycystic Kidney Disease, Moeka Nakashima; Naoko Suga; Yuka Ikeda; Sayuri Yoshikawa; Satoru Matsuda, Polycystic kidney disease (PKD) is the most common genetic form of chronic kidney disease (CKD), and it involves the development of multiple kidney cysts. Not enough medical breakthroughs have been made against PKD, a condition which features regional hypoxia and activation of the hypoxia-inducible factor (HIF) pathway. The following pathology of CKD can severely instigate kidney damage and/or renal failure. Significant evidence verifies an imperative role for mitophagy in normal kidney physiology and the pathology of CKD and/or PKD. Mitophagy serves as important component of mitochondrial quality control by removing impaired/dysfunctional mitochondria from the cell to warrant redox homeostasis and sustain cell viability. Interestingly, treatment with the peroxisome proliferator-activated receptor-α (PPAR-α) agonist could reduce the pathology of PDK and might improve the renal function of the disease via the modulation of mitophagy, as well as the condition of gut microbiome. Suitable modulation of mitophagy might be a favorable tactic for the prevention and/or treatment of kidney diseases such as PKD and CKD., Feb. 2024, 14, 2, 10.3390/biom14020207

Non-coding RNA, Circular RNAs, Noncoding RNAs, and N6-methyladenosine Involved in the Development of MAFLD, Moeka Nakashima; Naoko Suga; Yuka Ikeda; Sayuri Yoshikawa; Satoru Matsuda, Noncoding RNAs (ncRNAs), including circular RNAs (circRNAs) and N6-methyladenosine (m6A), have been shown to play a critical role in the development of various diseases including obesity and metabolic disorder-associated fatty liver disease (MAFLD). Obesity is a chronic disease caused by excessive fat accumulation in the body, which has recently become more prevalent and is the foremost risk factor for MAFLD. Causes of obesity may involve the interaction of genetic, behavioral, and social factors. m6A RNA methylation might add a novel inspiration for understanding the development of obesity and MAFLD with post-transcriptional regulation of gene expression. In particular, circRNAs, microRNAs (miRNAs), and m6A might be implicated in the progression of MAFLD. Interestingly, m6A modification can modulate the translation, degradation, and other functions of ncRNAs. miRNAs/circRNAs can also modulate m6A modifications by affecting writers, erasers, and readers. In turn, ncRNAs could modulate the expression of m6A regulators in different ways. However, there is limited evidence on how these ncRNAs and m6A interact to affect the promotion of liver diseases. It seems that m6A can occur in DNA, RNA, and proteins that may be associated with several biological properties. This study provides a mechanistic understanding of the association of m6A modification and ncRNAs with liver diseases, especially for MAFLD. Comprehension of the association between m6A modification and ncRNAs may contribute to the development of treatment tactics for MAFLD., Feb. 2024, 10, 1, 10.3390/ncrna10010011

International journal of physiology, pathophysiology and pharmacology, Caveolae with serotonin and NMDA receptors as promising targets for the treatment of Alzheimer's disease., Moeka Nakashima; Naoko Suga; Akari Fukumoto; Sayuri Yoshikawa; Satoru Matsuda, Alzheimer's disease is the most general type of cognitive impairments. Until recently, strategies that prevent its clinical progression have remained more elusive. Consequently, research direction should be for finding effective neuroprotective agents. It has been suggested oxidative stress, mitochondrial injury, and inflammation level might lead to brain cell death in many neurological disorders. Therefore, several autophagy-targeted bioactive compounds may be promising candidate therapeutics for the prevention of brain cell damage. Interestingly, some risk genes to Alzheimer's disease are expressed within brain cells, which may be linked to cholesterol metabolism, lipid transport, endocytosis, exocytosis and/or caveolae formation, suggesting that caveolae may be a fruitful therapeutic target to improve cognitive impairments. This review would highlight the latest advances in therapeutic technologies to improve the treatment of Alzheimer's disease. In particular, a paradigm that serotonin and N-methyl-d-aspartate (NMDA) receptors agonist/antagonist within caveolae structure might possibly improve the cognitive impairment. Consequently, cellular membrane biophysics should improve our understanding of the pathology of the cognitive dysfunction associated with Alzheimer's disease. Here, this research direction for the purpose of therapy may open the potential to move a clinical care toward disease-modifying treatment strategies with certain benefits for patients., 2024, 16, 5, 96, 110, Scientific journal, True, 10.62347/MTWV3745

International journal of physiology, pathophysiology and pharmacology, Comprehension of gut microbiota and microRNAs may contribute to the development of innovative treatment tactics against metabolic disorders and psychiatric disorders., Moeka Nakashima; Naoko Suga; Akari Fukumoto; Sayuri Yoshikawa; Satoru Matsuda, Metabolic syndrome is a group of pathological disorders increasing the risk of serious diseases including cardiovascular disease, stroke, type 2 diabetes. Global widespread of the metabolic syndrome has put a heavy social burden. Interestingly, a crucial link between the metabolic syndrome and a psychiatric disorder may frequently coexist, in which certain shared mechanisms might play a role for the pathogenesis. In fact, some microRNAs (miRNAs) have been detected in the overlap pathology, suggesting a common molecular mechanism for the development of both disorders. Subsequent studies have revealed that these miRNAs and several metabolites of gut microbiota such as short chain fatty acids (SCFAs) might be involved in the development of both disorders, in which the association between gut and brain might play key roles with engram memory for the modulation of immune cells. Additionally, the correlation between brain and immunity might also influence the development of several diseases/disorders including metabolic syndrome. Brain could possess several inflammatory responses as an information of pathological images termed engrams. In other words, preservation of the engram memory might be achieved by a meta-plasticity mechanism that shapes the alteration of neuron linkages for the development of immune-related diseases. Therefore, it might be rational that metabolic syndrome and psychiatric disorders may belong to a group of immune-related diseases. Disrupting in gut microbiota may threaten the body homeostasis, leading to initiate a cascade of health problems. This concept may contribute to the development of superior therapeutic application with the usage of some functional components in food against metabolic and psychiatric disorders. This paper reviews advances in understanding the regulatory mechanisms of miRNAs with the impact to gut, liver and brain, deliberating the probable therapeutic techniques against these disorders., 2024, 16, 6, 111, 125, Scientific journal, True, 10.62347/WAZH2090

Microorganisms, MDPI AG, Efficacy of Life Protection Probably from Newly Isolated Bacteria against Cisplatin-Induced Lethal Toxicity, Yuka Ikeda; Naoko Suga; Satoru Matsuda, Cisplatin may be commonly used in chemotherapy against various solid tumors. However, cisplatin has a limited safety range with serious side effects, which may be one of the dose-restraining reasons for cisplatin. A favorable therapeutic approach is immediately required for ameliorating cisplatin-induced toxicity. In the present study, the potential protective effects of certain bacteria have been investigated at the lethal dosage of cisplatin in mice experimental models. Treated under the highest dosage of cisplatin, treatment of certain commensal bacteria could significantly increase the survival rate. In addition, our findings revealed that probiotic supplementation of these bacteria could result in the attenuation of the damage appearance on the kidney as well as the alteration of several antioxidant-related gene expressions, including SOD1, SOD2, SOD3, Nrf2, and/or HO-1 genes in the high dosage of cisplatin-treated mice. In short, acute kidney injury in mice was induced by a single dose of cisplatin 11 or 15 mg/kg intraperitoneally. Then, peroral administration of newly isolated bacteria could protect against the cisplatin-induced injury, probably by decreasing oxidative stress. Therefore, the data shown here might suggest that the usage of certain probiotic supplementation could contribute to the life protection of patients suffering from severe toxicity of cisplatin. However, the molecular mechanisms need to be further explored., 06 Sep. 2023, 11, 9, 2246, 2246, Scientific journal, 10.3390/microorganisms11092246

Genes, MDPI AG, Non-Coding RNAs and Gut Microbiota in the Pathogenesis of Cardiac Arrhythmias: The Latest Update, Naoko Suga; Yuka Ikeda; Sayuri Yoshikawa; Kurumi Taniguchi; Haruka Sawamura; Satoru Matsuda, Non-coding RNAs (ncRNAs) are indispensable for adjusting gene expression and genetic programming throughout development and for health as well as cardiovascular diseases. Cardiac arrhythmia is a frequent cardiovascular disease that has a complex pathology. Recent studies have shown that ncRNAs are also associated with cardiac arrhythmias. Many non-coding RNAs and/or genomes have been reported as genetic background for cardiac arrhythmias. In general, arrhythmias may be affected by several functional and structural changes in the myocardium of the heart. Therefore, ncRNAs might be indispensable regulators of gene expression in cardiomyocytes, which could play a dynamic role in regulating the stability of cardiac conduction and/or in the remodeling process. Although it remains almost unclear how ncRNAs regulate the expression of molecules for controlling cardiac conduction and/or the remodeling process, the gut microbiota and immune system within the intricate networks might be involved in the regulatory mechanisms. This study would discuss them and provide a research basis for ncRNA modulation, which might support the development of emerging innovative therapies against cardiac arrhythmias., 30 Aug. 2023, 14, 9, 1736, 1736, Scientific journal, 10.3390/genes14091736

Neurology International, MDPI AG, In Search of a Function for the N6-Methyladenosine in Epitranscriptome, Autophagy and Neurodegenerative Diseases, Naoko Suga; Yuka Ikeda; Sayuri Yoshikawa; Kurumi Taniguchi; Haruka Sawamura; Satoru Matsuda, Changes in epitranscriptome with N6-methyladenine (m6A) modification could be involved in the development of multiple diseases, which might be a prevalent modification of messenger RNAs (mRNAs) in eukaryotes. The m6A modification might be performed through the action of methyltransferases, demethylases, and methylation-binding proteins. Importantly, the m6A methylation may be associated with various neurological disorders including Alzheimer’s disease (AD), Parkinson’s disease (PD), depression, aging-related diseases, and/or aging itself. In addition, the m6A methylation might functionally regulate the eukaryotic transcriptome by influencing the splicing, export, subcellular localization, translation, stability, and decay of mRNAs. Neurodegenerative diseases may possess a wide variety of phenotypes, depending on the neurons that degenerate on occasion. Interestingly, an increasing amount of evidence has indicated that m6A modification could modulate the expression of autophagy-related genes and promote autophagy in neuronal cells. Oxidative stresses such as reactive oxygen species (ROS) could stimulate the m6A RNA methylation, which may also be related to the regulation of autophagy and/or the development of neurodegenerative diseases. Both m6A modification and autophagy could also play critical roles in regulating the health condition of neurons. Therefore, a comprehensive understanding of the m6A and autophagy relationship in human diseases may benefit in developing therapeutic strategies in the future. This paper reviews advances in the understanding of the regulatory mechanisms of m6A modification in the occurrence and development of neurodegenerative diseases and/or aging, discussing the possible therapeutic procedures related to mechanisms of m6A RNA methylation and autophagy., 10 Aug. 2023, 15, 3, 967, 979, Scientific journal, 10.3390/neurolint15030062

LWT, Elsevier BV, Thermal stability of cricket powder and its effects on antioxidant activity, physical, and sensory properties of rice crackers, Naoko Suga; Eri Tsumura; Yuzuka Naito; Ikue Hamaguchi; Satoru Matsuda; Kyuichi Kawabata; Kaoru Sakamoto, Aug. 2023, 186, 115267, 115267, Scientific journal, 10.1016/j.lwt.2023.115267

Non-coding RNA, CircRNAs and RNA-Binding Proteins Involved in the Pathogenesis of Cancers or Central Nervous System Disorders., Yuka Ikeda; Sae Morikawa; Moeka Nakashima; Sayuri Yoshikawa; Kurumi Taniguchi; Haruka Sawamura; Naoko Suga; Ai Tsuji; Satoru Matsuda, Circular RNAs (circRNAs), a newly recognized group of noncoding RNA transcripts, have established widespread attention due to their regulatory role in cell signaling. They are covalently closed noncoding RNAs that form a loop, and are typically generated during the splicing of precursor RNAs. CircRNAs are key post-transcriptional and post-translational regulators of gene expression programs that might influence cellular response and/or function. In particular, circRNAs have been considered to function as sponges of specific miRNA, regulating cellular processes at the post-transcription stage. Accumulating evidence has shown that the aberrant expression of circRNAs could play a key role in the pathogenesis of several diseases. Notably, circRNAs, microRNAs, and several RNA-binding proteins, including the antiproliferative (APRO) family proteins, could be indispensable gene modulators, which might be strongly linked to the occurrence of diseases. In addition, circRNAs have attracted general interest for their stability, abundance in the brain, and their capability to cross the blood-brain barrier. Here, we present the current findings and theragnostic potentials of circRNAs in several diseases. With this, we aim to provide new insights to support the development of novel diagnostic and/or therapeutic strategies for these diseases., 31 Mar. 2023, 9, 2, Scientific journal, True, 10.3390/ncrna9020023

Exploration of Medicine, Roles of poly(ADP-ribose) polymerase 1 and mitophagy in progeroid syndromes as well as physiological ageing, Naoko Suga; Yuka Ikeda; Sayuri Yoshikawa; Satoru Matsuda, Progeroid syndromes are characterized by clinical signs of premature ageing, which may contain several diseases such as Werner syndrome, Bloom syndrome, Rothmund-Thomson syndrome, Hutchinson-Gilford progeria syndrome, and Cockayne syndrome. These disorders may also exhibit some pathological involvements reminiscent of primary mitochondrial diseases. Emerging evidence has linked mitochondria even to physiological ageing. In addition, alterations in the maintenance pathway of mitochondria have been also deliberated as relevant in age-related diseases. In particular, mitophagy and its regulatory pathway might be key process for the homeostasis of mitochondria. Therefore, chronic DNA damage and/or the activation of poly[adenosine diphosphate (ADP)-ribose] polymerase 1 (PARP1) could be a threat to the mitochondrial alterations. The PARP1 is an enzyme responding to the DNA damage, which might be also involved in the mitophagy. Interestingly, the PARP1 has been reported to play an important role in the longevity of lifespan, which has attracted growing attention with the social development. This review may provide a rationalized overview of the involvement of mitochondrial oxidative stresses in genetically defined accelerated ageing, progeroid syndromes, physiological ageing, and/or age-related diseases for the innovative therapeutic approaches., 2023, 4, 5, 822, 838, 10.37349/emed.2023.00180

Refereed, Jul. 2021, 54, 4, 186, 192

Journal of clinical biochemistry and nutrition, Luteolin suppresses 5-hydroxytryptamine elevation in stimulated RBL-2H3 cells and experimental colitis mice., Naoko Suga; Akira Murakami; Hideyuki Arimitsu; Toshiyuki Nakamura; Yoshimasa Nakamura; Yoji Kato, Increased 5-hydroxytryptamine may be associated with the development and progression of inflammatory bowel disease. In this study, we examined the suppressive effect of flavonoids on the increased intra- and extracellular 5-hydroxytryptamine levels in rat mast RBL-2H3 cells, known to produce 5-hydroxytryptamine by the phorbol 12-myristate 13-acetate stimulation. Among the flavonoids examined, luteolin and quercetin significantly reduced the cellular 5-hydroxytryptamine concentration. Gene and protein expression analyses revealed that luteolin significantly suppressed cellular tryptophan hydroxylase 1 expression induced by phorbol 12-myristate 13-acetate stimulation. Mitogen-activated protein kinase/extracellular signal-regulated kinase signaling was also suppressed by luteolin, suggesting that this pathway is one of targets of 5-hydroxytryptamine modulation by luteolin. An in vivo experimental colitis model was prepared by administering 2.5% dextran sodium sulfate in drinking water to C57BL/6 mice for seven days. The ingestion of 0.1% dietary luteolin suppressed the increasing 5-hydroxytryptamine in the colorectal mucosa. In conclusion, luteolin possesses a suppressive effect on extensive 5-hydroxytryptamine formation in both experimental RBL-2H3 cells and colitis models., Jul. 2021, 69, 1, 20, 27, Scientific journal, False, 10.3164/jcbn.20-192

Journal of clinical biochemistry and nutrition, Elevation of the serotonin-derived quinone, tryptamine-4,5-dione, in the intestine of ICR mice with dextran sulfate-induced colitis., Naoko Suga; Akira Murakami; Hideyuki Arimitsu; Kazuya Shiogama; Sarasa Tanaka; Mikiko Ito; Yoji Kato, Inflammatory bowel diseases, including Crohn's disease and ulcerative colitis, are chronic inflammatory disorders associated with oxidative stress. The intestines produce 5-hydroxytryptamine that may negatively affect disease state under inflammatory conditions when overproduced. 5-Hydroxytryptamine is a substrate for myeloperoxidase and is converted into reactive tryptamine-4,5-dione. Here, an experimental colitis model was established through oral administration of 5% dextran sulfate sodium to ICR mice for 7 days. Furthermore, the formation of tryptamine-4,5-dione in the colorectal mucosa/submucosa and colorectal tissue was analyzed by chemical and immunochemical methodologies. First, free tryptamine-4,5-dione in the homogenate was chemically trapped by o-phenylenediamine and analyzed as the stable phenazine derivative. Tryptamine-4,5-dione localization as adducted proteins in the colorectal tissue was immunohistochemically confirmed, and as demonstrated by both methods, this resulted in the significant increase of tryptamine-4,5-dione in dextran sulfate sodium-challenged mice compared with control mice. Immunohistochemical staining confirmed tryptamine-4,5-dione-positive staining at the myeloperoxidase accumulation site in dextran sulfate sodium-challenged mice colorectal tissue. The tryptamine-4,5-dione locus in the mice was partly matched with that of a specific marker for myeloperoxidase, halogenated tyrosine. Overall, the results possibly indicate that tryptamine-4,5-dione is generated by neutrophil myeloperoxidase in inflammatory tissue and may contribute to the development of inflammatory bowel disease., Jul. 2021, 69, 1, 61, 67, Scientific journal, False, 10.3164/jcbn.20-161

Food chemistry, Methylglyoxal binds to amines in honey matrix and 2'-methoxyacetophenone is released in gaseous form into the headspace on the heating of manuka honey., Yoji Kato; Yui Kishi; Yayako Okano; Masaki Kawai; Michiyo Shimizu; Naoko Suga; Chisato Yakemoto; Mai Kato; Akika Nagata; Noriyuki Miyoshi, Reports on the thermal stability of manuka honey in terms of food processing have been few. This study investigated changes in nine characteristic chemicals of manuka honey during heating. Among these, methylglyoxal (MGO) and 2'-methoxyacetophenone (MAP) were significantly decreased by heating at 90 °C. To elucidate the mechanism for this decrease, artificial honey was prepared from sugars and water with MAP or MGO and then heated. The decrease of MGO was enhanced with l-proline, lysine, or arginine derivatives, accompanied by formation of 2-acetyl-1-pyrroline, MGO-derived lysine dimer, or argpyrimidine, respectively, suggesting that an amino-carbonyl reaction is one pathway for the loss of MGO. The decrease of MAP in the artificial honey depended on the volume of headspace in a vessel. MAP from heated manuka honey was also detected in the gas phase, indicating that MAP was vaporized. Heating could thus reduce the beneficial and/or signature molecules in honey., 01 Feb. 2021, 337, 127789, 127789, Scientific journal, True, 10.1016/j.foodchem.2020.127789

Journal of clinical biochemistry and nutrition, Covalent adduction of endogenous and food-derived quinones to a protein: its biological significance., Yoji Kato; Naoko Suga, There are many chemically reactive compounds, including quinone, in living systems and also food. Even after the ingestion of food polyphenols, quinones derived from catechol moieties could form endogenously in the body. Dopaquinone, dopamine quinone, estrogen-derived quinones, tryptamine-4,5-dione, and ubiquinone are examples of an endogenous quinone. These indicate that quinone is ubiquitously formed or present in living systems and food. Quinones can induce a variety of hazardous effects and also could have beneficial physiological effects. This review focuses on the chemical reactivity of quinone toward a biomolecule and its biological action., May 2018, 62, 3, 213, 220, Scientific journal, False, 10.3164/jcbn.18-26

Free radical research, Cytotoxic and cytoprotective effects of tryptamine-4,5-dione on neuronal cells: a double-edged sword., Naoko Suga; Akira Murakami; Yoshimasa Nakamura; Akari Ishisaka; Noritoshi Kitamoto; Mikiko Ito; Yoji Kato, Serotonin (5-hydroxytryptamine) is a putative substrate for myeloperoxidase, which may convert it into the reactive quinone tryptamine-4,5-dione (TD). In this study, we found that the viability of human SH-SY5Y neuroblastoma cells treated with 25 μM TD was increased to approximately 117%. On the other hand, the cell viability was significantly decreased by exposure to TD (150-200 μM), with an increase in intracellular reactive oxygen species (ROS). Interestingly, pre-treatment of SH-SY5Y cells with 100 μM TD prevented cell death and suppressed intracellular ROS generation evoked by the addition of hydrogen peroxide (H2O2). Expression of the phase-II antioxidant enzyme NAD(P)H: quinone oxidoreductase 1 and haem oxygenase 1 were upregulated by TD at a concentration of 50-100 μM. Nuclear factor erythroid 2-related factor 2 (Nrf2), the regulator of these enzyme, was translocated from the cytosol to the nucleus by 100 μM TD. In summary, moderate concentrations of TD may increase the self-defence capacity of neuronal cells against oxidative stress., May 2017, 51, 5, 545, 553, Scientific journal, True, 10.1080/10715762.2017.1331038

Free radical biology & medicine, A novel quinone derived from 5-hydroxyindoleacetic acid reacts with protein: Possible participation of oxidation of serotonin and its metabolite in the development of atherosclerosis., Yoji Kato; Kota Oki; Naoko Suga; Shigeki Ono; Akari Ishisaka; Yoko Miura; Satoshi Kanazawa; Michitaka Naito; Noritoshi Kitamoto; Anthony J Kettle, The modification of 5-hydroxyindoleacetic acid (5HIAA) by myeloperoxidase with a xanthine oxidase system was investigated by chromatographic analyses. Two major products were identified as a dimer and quinone (indoleacetate dione) of 5HIAA. The formation of a quinone moiety was also confirmed by chemical trapping with o-phenylenediamine. In the presence of N-acetyl-cysteine (NAC), a quinone-NAC adduct was formed. When glyceraldehyde 3-phosphate dehydrogenase was exposed to the myeloperoxidase system with 5HIAA, quinone adducts were formed on the protein molecule. A monoclonal antibody was prepared using a quinone-modified protein as an immunogen to immunochemically detect the quinone on a protein. The established antibody recognized the quinone-NAC adduct, quinone-modified poly-L-lysine, and quinone-modified low-density lipoprotein. Quinone-modified proteins in human atherosclerotic lesions were immunohistochemically observed using the established antibody to the quinone and also a monoclonal antibody to tryptamine dione-modified protein, suggesting an occurrence of in vivo oxidation of serotonin and 5HIAA, accompanied by covalent adduction to biomolecules., Dec. 2016, 101, 500, 510, Scientific journal, True, 10.1016/j.freeradbiomed.2016.11.023

International Journal of Molecular Sciences, Caveolin and NOS in the Development of Muscular Dystrophy, Moeka Nakashima; Naoko Suga; Sayuri Yoshikawa; Satoru Matsuda, Caveolin is a structural protein within caveolae that may be involved in transmembrane molecular transport and/or various intercellular interactions within cells. Specific mutations of caveolin-3 in muscle fibers are well known to cause limb–girdle muscular dystrophy. Altered expression of caveolin-3 has also been detected in Duchenne muscular dystrophy, which may be a part of the pathological process leading to muscle weakness. Interestingly, it has been shown that the renovation of nitric oxide synthase (NOS) in sarcolemma with muscular dystrophy could improve muscle health, suggesting that NOS may be involved in the pathology of muscular dystrophy. Here, we summarize the notable function of caveolin and/or NOS in skeletal muscle fibers and discuss their involvement in the pathology as well as possible tactics for the innovative treatment of muscular dystrophies., Aug. 2024, 25, 16, True, 10.3390/ijms25168771

Molecules, Caveolae with GLP-1 and NMDA Receptors as Crossfire Points for the Innovative Treatment of Cognitive Dysfunction Associated with Neurodegenerative Diseases, Moeka Nakashima; Naoko Suga; Sayuri Yoshikawa; Satoru Matsuda, Some neurodegenerative diseases may be characterized by continuing behavioral and cognitive dysfunction that encompasses memory loss and/or apathy. Alzheimer’s disease is the most typical type of such neurodegenerative diseases that are characterized by deficits of cognition and alterations of behavior. Despite the huge efforts against Alzheimer’s disease, there has yet been no successful treatment for this disease. Interestingly, several possible risk genes for cognitive dysfunction are frequently expressed within brain cells, which may also be linked to cholesterol metabolism, lipid transport, exosomes, and/or caveolae formation, suggesting that caveolae may be a therapeutic target for cognitive dysfunctions. Interestingly, the modulation of autophagy/mitophagy with the alteration of glucagon-like peptide-1 (GLP-1) and N-methyl-d-aspartate (NMDA) receptor signaling may offer a novel approach to preventing and alleviating cognitive dysfunction. A paradigm showing that both GLP-1 and NMDA receptors at caveolae sites may be promising and crucial targets for the treatment of cognitive dysfunctions has been presented here, which may also be able to modify the progression of Alzheimer’s disease. This research direction may create the potential to move clinical care toward disease-modifying treatment strategies with maximal benefits for patients without detrimental adverse events for neurodegenerative diseases., Aug. 2024, 29, 16, True, 10.3390/molecules29163922

Abstracts of the Annual Meeting of the Japan Society of Cookery Science, The Japan Society of Cookery Science, The study on brown rice processing to enhance the prebiotic potential, Suga Naoko; Nuka Erika; Uchida Haruka; Kawabata Kyuichi; Sakamoto Kaoru, Sep. 2022, 33, 8, 10.11402/ajscs.33.0_8

Abstracts of the Annual Meeting of the Japan Society of Cookery Science, The Japan Society of Cookery Science, Cooking properties and antioxidative activity of rice crackers with cricket powder, Tsumura Eri; Naito Yuzuka; Sakamoto Kaoru; Suga Naoko, Sep. 2022, 33, 173, 10.11402/ajscs.33.0_173

978-4-06-534135-3

Naoko Suga, Hideyuki Arimitsu, Akira Murakami, Yoji Kato, The 7th International Conference on Food Factors, Suppressive effects of luteolin on serotonin production in RBL-2H3 cells, Dec. 2019

Yoji Kato, Sae Fujisjima, Naoko Suga, Aoi Sugimoto,  Makoto Naoi, Wakako Maruyama, The 7th International Conference on Food Factors, Irreversible inhibition  of monoamine oxidases by serotonin-derived quinones, Dec. 2019

Yui Kishi, Masaki Kawai, Yayako Okano, Naoko Suga, Mai Kato, Akika Nagata, Noriyuki Miyoshi, Yoji Kato, The 7th International Conference on Food Factors, Loss of key components, methylglyoxal and 2′-methoxyacetophenone, in manuka honey by heat processing, Dec. 2019

Naoko Suga, Akira Murakami, Yoji Kato, The 9th Biennial Meeting of Society for Free Radical Research-Asia, Oxidation of serotonin metabolite, 5-hydroxyindoleacetic acid, in the intestinal mucosa - A model study using intestine homogenate -, Apr. 2019

Naoko Suga, Akari Ishisaka, Noritoshi Kitamoto, Mikiko Ito, Akira Murakami, Yoshimasa Nakamura, Yoji Kato, The Society for Free Radical Research Australasia & Japan 7th Joint Meeting, Modification of cellular proteins and induction of self-defense genes expressions by tryptamine-4,5-dione, a serotonin oxidation product, Dec. 2015

Naoko Suga, Akari Ishisaka, Noritoshi Kitamoto, Akira Murakami, Yoshimasa Nakamura, Yoji Kato, The 6th International Conference on Food Factor, Effect of quinone derived from 5-hydroxytryptamine on expression of genes in SH-SY5Y neuroblastoma cells, Nov. 2015

Dec. 2018

Sep. 2016

Dec. 2015

Young Scientist Oral Presentation Award, The Society for Free Radical Research Australasia, Dec. 2015

Nov. 2015

Poster Award, International Conference on Food Factors（ICoFF）, Nov. 2015