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  <channel rdf:about="https://oak.ulsan.ac.kr/handle/2021.oak/8280">
    <title>Repository Collection: null</title>
    <link>https://oak.ulsan.ac.kr/handle/2021.oak/8280</link>
    <description />
    <items>
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        <rdf:li rdf:resource="https://oak.ulsan.ac.kr/handle/2021.oak/19830" />
        <rdf:li rdf:resource="https://oak.ulsan.ac.kr/handle/2021.oak/19301" />
        <rdf:li rdf:resource="https://oak.ulsan.ac.kr/handle/2021.oak/19011" />
        <rdf:li rdf:resource="https://oak.ulsan.ac.kr/handle/2021.oak/19010" />
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    <dc:date>2026-04-05T04:45:02Z</dc:date>
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  <item rdf:about="https://oak.ulsan.ac.kr/handle/2021.oak/19830">
    <title>Protective effects of taurine and betaine against neurotoxicity via inhibition of endoplasmic reticulum stress and inflammation signaling in the brain of mice fed a Western diet</title>
    <link>https://oak.ulsan.ac.kr/handle/2021.oak/19830</link>
    <description>Title: Protective effects of taurine and betaine against neurotoxicity via inhibition of endoplasmic reticulum stress and inflammation signaling in the brain of mice fed a Western diet
Author(s): Je Won Ko; Younji Lee; Yumi Jang; Young Hye Kwon
Abstract: Western diet (WD) has been shown to impair liver functions via endoplasmic reticulum (ER) stress and oxidative stress. Although osmolytes prevent liver dysfunction, little is known about the mechanisms by which they exert neuroprotective effects against WD-induced damage. We investigated neuroprotective effects of osmolytes and determined the involvement of inflammasome-mediated inflammation in liver and brain. Mice were fed a control diet, WD, or WD with taurine or betaine. Osmolyte supplementation attenuated serum lipid peroxidation and inflammatory cytokine levels in WD-fed mice. Oxidative stress, inflammasome-mediated inflammation, ER stress, and insulin resistance were lower in liver and brain of mice fed osmolyte-supplemented diet than in those fed WD. Moreover, they activated brain-derived neurotrophic factor signaling and decreased β-amyloid deposition and tau hyperphosphorylation in the brain. These data implicate that osmolytes might be promising neuroprotective dietary supplements for WD-induced brain damage, as well as for previously reported genetically and chemically induced brain damage.</description>
    <dc:date>2023-12-31T15:00:00Z</dc:date>
  </item>
  <item rdf:about="https://oak.ulsan.ac.kr/handle/2021.oak/19301">
    <title>Filbertone Reduces Senescence in C2C12 Myotubes Treated with Doxorubicin or H2O2 through MuRF1 and Myogenin</title>
    <link>https://oak.ulsan.ac.kr/handle/2021.oak/19301</link>
    <description>Title: Filbertone Reduces Senescence in C2C12 Myotubes Treated with Doxorubicin or H2O2 through MuRF1 and Myogenin
Author(s): Sumin Jung; Byungyong Ahn
Abstract: It has been demonstrated that filbertone, the principal flavor compound of hazelnuts, exhibits preventive effects against hypothalamic inflammation, obesity, neurodegenerative diseases, and muscle lipid accumulation. However, its influence on muscle aging has yet to be elucidated. The objective of this study was to investigate the effects of filbertone on muscle aging in C2C12 myotubes subjected to senescence induction by either doxorubicin or hydrogen peroxide. To ascertain the mechanisms by which filbertone exerts its effects, we conducted a series of experiments, including Western blot analysis, reverse transcription quantitative polymerase chain reaction (qRT-PCR), and senescence-associated β-galactosidase (SA-β-gal) staining. Filbertone was markedly observed to decrease not only the protein levels of p53 (p &lt; 0.01) in senescence-induced skeletal muscle cells, but also the gene expression levels of p21 (p &lt; 0.05), a direct target of p53. The expression of muscle-related genes, including myogenin and muscle RING-finger protein-1 (MuRF1), was found to be significantly enhanced in senescent muscle cells following treatment with filbertone (p &lt; 0.05). In addition, the number of senescent skeletal muscle cells exhibiting β-galactosidase activity was found to be markedly reduced in the presence of filbertone (p &lt; 0.01). Collectively, these findings suggest that filbertone plays a pivotal role in the regulation of muscle aging.</description>
    <dc:date>2023-12-31T15:00:00Z</dc:date>
  </item>
  <item rdf:about="https://oak.ulsan.ac.kr/handle/2021.oak/19011">
    <title>Filbertone-Induced Nrf2 Activation Ameliorates Neuronal Damage via Increasing BDNF Expression</title>
    <link>https://oak.ulsan.ac.kr/handle/2021.oak/19011</link>
    <description>Title: Filbertone-Induced Nrf2 Activation Ameliorates Neuronal Damage via Increasing BDNF Expression
Author(s): Jeong Heon Gong; Chu-Sook Kim; Jeongmin Park; Soeun Kang; Yumi Jang; Min-Seon Kim; Hun Taeg Chung; Yeonsoo Joe; Rina Yu
Abstract: Neurotrophic factors are endogenous proteins that promote the survival of various neuronal cells. Increasing evidence has suggested a key role for brain-derived neurotrophic factor (BDNF) in the dopaminergic neurotoxicity associated with Parkinson's Disease (PD). This study explores the therapeutic potential of filbertone, a bioactive compound found in hazelnuts, in neurodegeneration, focusing on its effects on neurotrophic factors and the nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway. In our study, filbertone markedly elevated the expression of neurotrophic factors, including BDNF, Glial cell line-Derived Neurotrophic Factor (GDNF), and Nerve Growth Factor (NGF), in human neuroblastoma SH-SY5Y cells, mouse astrocyte C8-D1A cells, and mouse hypothalamus mHypoE-N1 cells. Moreover, filbertone effectively countered neuroinflammation and reversed the decline in neurotrophic factors and Nrf2 activation induced by a high-fat diet (HFD) in neurodegeneration models. The neuroprotective effects of filbertone were further validated in models of neurotoxicity induced by palmitic acid (PA) and the neurotoxin MPTP/MPP+, where it was observed to counteract PA and MPTP/MPP+-induced decreases in cell viability and neuroinflammation, primarily through the activation of Nrf2 and the subsequent upregulation of BDNF and heme oxygenase-1 expression. Nrf2 deficiency negated the neuroprotective effects of filbertone in MPTP-treated mice. Consequently, our finding suggests that filbertone is a novel therapeutic agent for neurodegenerative diseases, enhancing neuronal resilience through the Nrf2 signaling pathway and upregulation of neurotrophic factors.</description>
    <dc:date>2023-12-31T15:00:00Z</dc:date>
  </item>
  <item rdf:about="https://oak.ulsan.ac.kr/handle/2021.oak/19010">
    <title>The Role of Vitamin E Isoforms and Metabolites in Cancer Prevention: Mechanistic Insights into Sphingolipid Metabolism Modulation</title>
    <link>https://oak.ulsan.ac.kr/handle/2021.oak/19010</link>
    <description>Title: The Role of Vitamin E Isoforms and Metabolites in Cancer Prevention: Mechanistic Insights into Sphingolipid Metabolism Modulation
Author(s): 김춘영; 장유미
Abstract: Natural forms of vitamin E include four tocopherols and four tocotrienols (α, β, γ, and δ), which are essential as lipophilic antioxidants. Among these eight isoforms, α-tocopherol (αT), the predominant form of vitamin E found in tissues, has traditionally received the most attention in disease prevention research due to its robust antioxidant activity. However, recent studies suggest that other forms of vitamin E exhibit distinct and potentially more potent beneficial activities in disease prevention and treatment. These non-αT forms of vitamin E are metabolized in vivo, producing various metabolites, including 13'-carboxychromanol, though their biological roles remain largely unknown. Notably, sphingolipids, known for their significant roles in cancer biology, may be involved in the anticancer effects of vitamin E through the modulation of sphingolipid metabolism. This review focuses on the diverse biological activities of different vitamin E forms and their metabolites, particularly their anticancer effects, while highlighting the underlying mechanisms, including their novel impact on regulating sphingolipid pathways. By elucidating these interactions, we aim to provide a deeper understanding on the multifaceted roles of vitamin E in cancer prevention and therapy.</description>
    <dc:date>2023-12-31T15:00:00Z</dc:date>
  </item>
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