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Choi K.-C.,South Korean National Institute of Animal Science | Hwang J.-M.,Chonbuk National University | Bang S.-J.,Chonbuk National University | Son Y.-O.,University of Kentucky | And 6 more authors.
Pharmaceutical Biology | Year: 2013

Context: Recently, there has been renewed interest in barley (Hordeum vulgare L. Poaceae) as a functional food and for its medicinal properties. Objective: This study examines the anti-inflammatory potential of the active fractions of barley and the mechanisms involved. Materials and methods: The macrophages were exposed to 100 mg/mL of each of the barley extracts in the presence of 1 mg/mL lipopolysaccharide (LPS) and after 24 or 48 h of incubation, cells or culture supernatants were analyzed by various assays. The anti-inflammatory potential of barley fractions was also investigated using the LPS-injected septic mouse model. The active constituents in the fractions were identified using gas chromatography-mass spectrometry (GC-MS). Results: The active fractions, named F4, F7, F9 and F 12, inhibited almost completely the LPS-induced production of nitric oxide (NO) and inducible NO synthase. Pre-treatment with these fractions at 100 mg/mL diminished the tumor necrosis factor-a (TNF-a) levels to 19.8, 3.5, 1.2 and 1.7 ng/mL, respectively, compared to LPS treatment alone (41.5 ng/mL). These fractions at 100 mg/mL also suppressed apparently the secretion of interleukin (IL)-6 and IL-1b and the DNA-binding activity of nuclear factor-kB in LPS-stimulated cells. Mice injected intraperitoneally with LPS (30 mg/kg BW) showed 20% survival at 48 h after injection, whereas oral administration of the fractions improved the survival rates to 80%. GC-MS analysis revealed the presence of the derivatives of benzoic and cinnamic acids and fatty acids in the fractions. Discussion and conclusion: The aerial parts of barley are useful as functional food to prevent acute inflammatory responses. © 2013 Informa Healthcare USA, Inc. Source


Kim K.-A.,Chonbuk National University | Lee S.-A.,Chonnam Techno College | Kim K.-H.,Chonbuk National University | Lee K.-S.,Korea Bone Bank Co | Lee J.-C.,Chonbuk National University
Food Science and Biotechnology | Year: 2013

Therapeutic irradiation can cause bone loss, whereas antioxidant supplementation is considered to attenuate irradiation-mediated damages. This study examined whether or not acteoside inhibits irradiation-mediated changes in viability and proliferation of MC3T3-E1 cells. X-ray radiation at >4 Gy not only decreased cell viability and DNA synthesis in the cells, but also increased intracellular levels of reactive oxygen species (ROS) and phosphorylated p66Shc protein. Irradiation at 8Gy also decreased intracellular levels of reduced glutathione (GSH) and induced G1 phase arrest of cell cycle progression with the attendant increase of p21 induction. Pretreatment with acteoside inhibited the irradiation-mediated decreases in viability and DNA synthesis by restoring the radiation-mediated changes in the levels of ROS, GSH, p21, and p-p66Shc to the untreated control levels. These inhibitory activities of acteoside were greater than that of a synthetic antioxidant compound or N-acetyl cysteine did. Collectively, acteoside treatment may prevent irradiation-induced oxidative damages to osteoblasts. © 2013 The Korean Society of Food Science and Technology and Springer Science+Business Media Dordrecht. Source


Lee D.,Chonbuk National University | Kook S.-H.,Chonbuk National University | Ji H.,Chonbuk National University | Lee S.-A.,Chonnam Techno College | And 3 more authors.
BMB Reports | Year: 2015

There are controversial findings regarding the roles of nuclear factor (erythroid-derived 2)-like 2 (Nrf2)/heme oxygenase-1 (HO-1) pathway on bone metabolism under oxidative stress. We investigated how Nrf2/HO-1 pathway affects osteoblast differentiation of MC3T3-E1 cells in response to hydrogen peroxide (H2O2), N-acetyl cysteine (NAC), or both. Exposing the cells to H2O2 decreased the alkaline phosphatase activity, calcium accumulation, and expression of osteoblast markers, such as osteocalcin and runt-related transcription factor-2. In contrast, H2O2 treatment increased the expression of Nrf2 and HO-1 in the cells. Treatment with hemin, a chemical HO-1 inducer, mimicked the inhibitory effect of H2O2 on osteoblast differentiation by increasing the HO-1 expression and decreasing the osteogenic marker genes. Pretreatment with NAC restored all changes induced by H2O2 to near normal levels in the cells. Collectively, our findings suggest that H2O2-mediated activation of Nrf2/HO-1 pathway negatively regulates the osteoblast differentiation, which is inhibited by NAC. © 2015 by the The Korean Society for Biochemistry and Molecular Biology. Source


Lee S.-A.,Chonbuk National University | Lee S.-A.,Chonnam Techno College | Son Y.-O.,University of Kentucky | Kook S.-H.,University of Pittsburgh | And 2 more authors.
Archives of Dermatological Research | Year: 2011

Ascorbic acid, a potential antioxidant, is known to inhibit melanogenesis. However, there are conflicting findings that ascorbic acid has very low stability and acts as a pro-oxidant, eventually increasing proliferation and melanin content in melanoma cells. In the present study, we explored the effects of ascorbic acid on the activity and expression of tyrosinase and melanin pigmentation in the presence and absence of α-melanocyte-stimulating hormone (α-MSH) using B16F10 melanoma cells. The mechanism by which ascorbic acid stimulated the expression of tyrosinase was also investigated. No inhibitory effect on melanin content was observed in ascorbic acid-treated cells, regardless of the presence of α-MSH. Ascorbic acid stimulated the activity and expression of tyrosinase and increased the expression of melanogenic regulatory factors, such as tyrosinase-related protein-1 (TRP-1), dihydroxyphenylalaminechrome tautomerase (TRP-2), and microphthalmia-associated transcription factor (MITF). Ascorbic acid also induced phosphorylation of p38 mitogen-activated protein kinase (MAPK). The inhibition of p38 MAPK pathway by SB203580 led to the suppression of tyrosinase, TRP-1, and TRP-2 expression in cells treated with ascorbic acid. Combined treatment with N-acetyl-L-cysteine and/or desferrioxamine mesylate attenuated the stimulating effect of ascorbic acid on tyrosinase activation in the cells. Collectively, ascorbic acid stimulates tyrosinase activity and expression in B16F10 cells via activation of p38 MAPK signaling and subsequent up-regulation of MITF, tyrosinase, and TRP expression. © 2011 Springer-Verlag. Source


Lu J.,Chonbuk National University | Yu J.-Y.,Korea Research Institute of Chemical Technology | Lim S.-S.,Chonbuk National University | Son Y.-O.,University of Kentucky | And 5 more authors.
Toxicology in Vitro | Year: 2013

Zearalenone (ZEN) and its metabolites are commonly found in many food commodities and are known to cause reproductive disorders and genotoxic effects. The major ZEN metabolites are α-zearalenol (α-ZOL) and β-zearalenol (β-ZOL). Although many studies have demonstrated the cytotoxic effects of these metabolites, the mechanisms by which α-ZOL or β-ZOL mediates their cytotoxic effects appear to differ according to cell type and the exposed toxins. We evaluated the toxicity of α-ZOL and β-ZOL on RAW264.7 macrophages and investigated the underlying mechanisms. β-ZOL not only more strongly reduced the viability of cells than did α-ZOL, but it also induced cell death mainly by apoptosis rather than necrosis. The ZEN metabolites induced loss of mitochondrial membrane potential (MMP), mitochondrial changes in Bcl-2 and Bax proteins, and cytoplasmic release of cytochrome c and apoptosis-inducing factor (AIF). Use of an inhibitor specific to c-Jun N-terminal kinase (JNK), p38 kinase or p53, but not pan-caspase or caspase-8, decreased the toxin-induced generation of reactive oxygen species (ROS) and also attenuated the α-ZOL- or β-ZOL-induced decrease of cell viability. Antioxidative enzyme or compounds such as catalase, acteoside, and (E)-1-(3,4-dihydroxyphenethyl)-3-(4-hydroxystyryl)urea suppressed the ZEN metabolite-mediated reduction of cell viability. Further, knockdown of AIF via siRNA transfection diminished the ZEN metabolite-induced cell death. Collectively, these results suggest that the activation of p53, JNK or p38 kinase by ZEN metabolites is the main upstream signal required for the mitochondrial alteration of Bcl-2/Bax signaling pathways and intracellular ROS generation, while MMP loss and nuclear translocation of AIF are the critical downstream events for ZEN metabolite-mediated apoptosis in macrophages. © 2013 Elsevier Ltd. Source

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