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Cheongju, South Korea

Cheongju University is a private university located in Cheongju City, the capital of North Chungcheong province, South Korea. The current president is Kim Yoon Bae. Wikipedia.

Obesity is closely associated with a state of chronic, low-grade inflammation characterized by abnormal cytokine production and activation of inflammatory signaling pathways in adipose tissue. Tumor necrosis factor (TNF)-α is chronically elevated in adipose tissues of obese rodents and humans. Increased levels of TNF-α are implicated in the induction of atherogenic adipokines, such as plasminogen activator inhibitor (PAI)-1, adipose-tissue-derived monocyte chemoattractant protein (MCP)-1, and interleukin (IL)-6. Aucubin, an iridoid glycoside existing in medicinal plants, has been reported to show an anti-inflammatory activity by suppression of TNF-α production in murine macrophages. The present study is aimed to investigate the effects of aucubin on TNF-α-induced atherogenic changes of the adipokines in differentiated 3T3-L1 cells. Aucubin significantly inhibited TNF-α-induced secretion and mRNA synthesis of the atherogenic adipokines including PAI-1, MCP-1, and IL-6. Further investigation of the molecular mechanism revealed that pretreatment with aucubin suppressed extracellular signal-regulated kinase (ERK) activation, inhibitory kappa Bα (IκBα) degradation, and subsequent nuclear factor kappa B (NF-κB) activation. These findings suggest that aucubin may improve obesity-induced atherosclerosis by attenuating TNF-α-induced inflammatory responses. © 2013 Elsevier Ltd. Source

Jung W.-W.,Cheongju University
International Journal of Molecular Medicine | Year: 2014

Apigenin, a plant-derived flavonoid, was investigated to determine whether it could influence hydrogen peroxide (H2O2)-induced oxidative damage and cellular dysfunction in the MC3T3-E1 mouse osteoblastic cell line. In the present study, osteoblastic cells were treated with H 2O2 in the presence or absence of apigenin. Cell viability, apoptosis, reactive oxygen species (ROS) production and mitochondrial membrane potential (ΔΨm) were subsequently examined. It was observed that H2O2 reduced cell survival and ΔΨm, while it markedly increased the intracellular levels of ROS and apoptosis. However, pretreatment of cells with apigenin attenuated all the H2O 2-induced effects. The antioxidants, catalase and N-acetyl-L-cysteine (NAC) also prevented H2O2-induced oxidative cell damage. In addition, treatment with apigenin resulted in a significant elevation of osteoblast differentiation genes including alkaline phosphatase (ALP), collagen, osteopontin (OPN), osteoprotegerin (OPG), bone sialoprotein (BSP), osterix (OSX) and osteocalcin (OC) and bone morphogenetic proteins (BMPs) genes (BMP2, BMP4 and BMP7). In the mechanistic studies of cell signaling by the antioxidative potential of apigenin, it was found that apigenin activated the H2O2-induced decreased expression of phosphatidylinositol 3′-kinase (PI3K), protein kinase B2 (AKT2) genes and extracellular signal-related kinase (EPK) 2, which are key regulators of survival-related signaling pathways. By contrast, there were no changes in the expression of nuclear facor-κB (NF-κB) and c-Jun N-terminal kinase (JNK) gene exposed to H2O2 in the present study. Apigenin also upregulated the gene expression of antioxidant enzymes, superoxide dismutase (SOD) 1, SOD2 and glutathione peroxidase (GPx) 1. Taken together, these results suggested that apigenin attenuated oxidative-induced cell damage in osteoblastic cells and may be useful for the treatment of oxidative-related bone disease. Source

Previous studies have shown that one of the primary causes of increased iron content in the brain may be the release of excess iron from intracellular iron storage molecules such as ferritin. Free iron generates ROS that cause oxidative cell damage. Carnosine and related compounds such as endogenous histidine dipetides have antioxidant activities. We have investigated the protective effects of carnosine and homocarnosine against oxidative damage of DNA induced by reaction of ferritin with H 2O 2. The results show that carnosine and homocarnosine prevented ferritin/H 2O 2-mediated DNA strand breakage. These compounds effectively inhibited ferritin/ H 2O 2-mediated hydroxyl radical generation and decreased the mutagenicity of DNA induced by the ferritin/H 2O 2 reaction. Our results suggest that carnosine and related compounds might have antioxidant effects on DNA under pathophysiological conditions leading to degenerative damage such as neurodegenerative disorders. Source

Lee S.,Cheongju University
Telematics and Informatics | Year: 2013

This study examines what factors lead to the adoption of the mobile e-book in South Korea. For this purpose, this research integrated the diffusion of innovation theory and technology acceptance model with the model of innovation resistance and applied this integrated model to the context of mobile e-book adoption. An online survey was administrated, and the data collected were analyzed with the structural equation model (SEM). Research results showed that individual innovativeness has a significant influence on perceived usefulness and perceived ease of use. It also revealed that both of perceived usefulness and perceived ease of use affect not only intention to use but also the innovation resistance. The innovation resistance has significant negative influence on the intention to use. Perceived risk of mobile e-books increases innovation resistance in a positive way. The implications of these results are discussed. © 2012 Elsevier Ltd. All rights reserved. Source

Acrolein is the most reactive aldehydic product of lipid peroxidation and is found to be elevated in the brain when oxidative stress is high. The effects of acrolein on the structure and function of human Cu,Zn-superoxide dismutase (SOD) were examined. When Cu,Zn-SOD was incubated with acrolein, the covalent crosslinking of the protein was increased, and the loss of enzymatic activity was increased in a dose-dependent manner. Reactive oxygen species (ROS) scavengers and copper chelators inhibited the acrolein-mediated Cu,Zn-SOD modification and the formation of carbonyl compound. The present study shows that ROS may play a critical role in acrolein-induced Cu,Zn-SOD modification and inactivation. When Cu,Zn-SOD that has been exposed to acrolein was subsequently analyzed by amino acid analysis, serine, histidine, arginine, threonine and lysine residues were particularly sensitive. It is suggested that the modification and inactivation of Cu,Zn-SOD by acrolein could be produced by more oxidative cell environments. © 2013 by the The Korean Society for Biochemistry and Molecular Biology. Source

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