Jin Tae Hong

Chonnam National University, Gwangju, Gwangju, South Korea

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Publications (317)886.91 Total impact

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    ABSTRACT: Alzheimer's disease (AD) is pathologically characterized by excessive accumulation of amyloid-beta (Aβ) peptide. Evidence suggests that amyloid accumulation can be caused by oxidative stress and inflammatory responses. In this study, we examined neuroprotective effects of thiacremonone, an anti-oxidant and anti-inflammatory compound isolated from garlic. Treatment of thiacremonone significantly attenuated cognitive impairments in amyloid precursor protein (APP)/presenilin 1 (PS1) double-mutant transgenic mice. In addition, activation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and extracellular signal-regulated kinase (ERK) pathways in the brain was potently inhibited by thiacremonone. We also observed that thiacremonone significantly inhibited activation of NF-κB and ERK pathways induced by H2O2 and Aβ1-42 in embryonic neuronal cells. Furthermore, thiacremonone augmented peroxiredoxin 6 (PRDX6) expression in vivo and in vitro associated with reduced oxidative stress of macromolecules such as protein and lipids. This study indicates that thiacremonone might exert memory improvement via stimulating anti-oxidant system. These multiple properties could attenuate Aβ accumulation and oxidative stress in Alzheimer's brains. Thus, these results suggest that thiacremonone might be useful to intervene development or progression of neurodegeneration in AD.
    Molecular Neurobiology 05/2015; DOI:10.1007/s12035-015-9208-0 · 5.29 Impact Factor
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    ABSTRACT: Recently, biphenolic components derived from the Magnolia family have been studied for anti-cancer, anti-stress, and anti-inflammatory pharmacological effects. However, the pharmacological mechanism of action of 4-O-methylhonokiol (MH) is not clear in oral cancer. The aim of this study was to investigate the role of MH in apoptosis and its molecular mechanism in oral squamous cell carcinoma (OSCC) cell lines, HN22 and HSC4, as well as tumor xenografts. Here, we demonstrated that MH decreased cell growth and induced apoptosis in HN22 and HSC4 cells through the regulation of specificity protein 1 (Sp1). We employed several experimental techniques such as MTS assay, DAPI staining, PI staining, Annexin-V/7-ADD staining, RT-PCR, western blot analysis, immunocytochemistry, immunohistochemistry, TUNEL assay and in vivo xenograft model analysis. MH inhibited Sp1 protein expression and reduced Sp1 protein levels via both proteasome-dependent protein degradation and inhibition of protein synthesis in HN22 and HSC4 cells; MH did not alter Sp1 mRNA levels. We found that MH directly binds Sp1 by Sepharose 4B pull-down assay and molecular modeling. In addition treatment with MH or knocking down Sp1 expression, suppressed oral cancer cell colony formation. Moreover, MH treatment effectively inhibited tumor growth and Sp1 levels in BALB/c nude mice bearing HN22 cell xenografts. These results indicated that MH inhibited cell growth, colony formation and also induced apoptosis via Sp1 suppression in OSCC cells and xenograft tumors. Thus MH is a potent anti-cancer drug candidate for oral cancer. Copyright © 2015. Published by Elsevier Ltd.
    The international journal of biochemistry & cell biology 05/2015; DOI:10.1016/j.biocel.2015.05.007 · 4.24 Impact Factor
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    ABSTRACT: Objectives This study aimed to investigate the beneficial effects of Cheonggukjang (CGK) manufactured by mixed culture of Bacillus subtilis MC31 and Lactobacillus sakei 383 on neurotoxic damages. Methods The specific aspects of brain functions were measured in ICR mice that had been pretreated for 4 weeks with three difference doses of CGK before trimethyltin (TMT) treatment. Results The short- and long-term memory loss induced by TMT treatment was significantly improved in the CGK-pretreated group in a dose-dependent manner. The number of dead cells in the granule cell layer of the dentate gyrus was decreased in the TMT/CGK-cotreated group relative to the TMT/vehicle-treated group, whereas significant suppression of acetylcholinesterase (AChE) activity was observed in the same group. Additionally, a dose-dependent increase in nerve growth factor (NGF) concentration, activation of the NGF receptor signaling pathway including the TrkA high affinity receptor and p75(NTR) low affinity receptor, and decline in Bax/Bcl-2 level was measured in all TMT/CGK-treated groups, although a decrease in the active form of caspase-3 was observed in the TMT/H-CGK-treated group. Furthermore, superoxide dismutase (SOD) activity was enhanced in the TMT/CGK-treated group, whereas the level of malondialdehyde (MDA), a marker of lipid peroxidation, was 43-58% lower in the TMT/CGK-treated group than the TMT/vehicle-treated group. Discussion These results demonstrate that CGK fermented by mixed culture of B. subtilis and L. sakei could exert a wide range of beneficial activities for neurodegenerative diseases, including Alzheimer, Parkinson, and Huntington disease.
    Nutritional Neuroscience 04/2015; DOI:10.1179/1476830515Y.0000000025 · 2.11 Impact Factor
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    ABSTRACT: Inflammation is associated with cancer-prone microenvironment, leading to cancer. IL-32 is expressed in chronic inflammation-linked human cancers. To investigate IL-32α in inflammation-linked colorectal carcinogenesis, we generated a strain of mice, expressing IL-32 (IL-32α-Tg). In IL-32α-Tg mice, azoxymethane (AOM)-induced colon cancer incidence was decreased, whereas expression of TNFR1 and TNFR1-medicated apoptosis was increased. Also, IL-32α increased ROS production to induce prolonged JNK activation. In colon cancer patients, IL-32α and TNFR1 were increased. These findings indicate that IL-32α suppressed colon cancer development by promoting the death signaling of TNFR1.
    Oncotarget 04/2015; · 6.63 Impact Factor
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    ABSTRACT: Naphthofuran compounds have been known to regulate HNF 4α which is associated with proliferation, progression and metastasis of HCC. In this study, we investigated whether N-(3,5-bis(trifluoromethyl)phenyl)-5-chloro-2,3-dihydronaphtho[1,2-b]furan-2-carboxamide (NHDC), a novel synthetic naphthofuran compound inhibits liver tumor growth through activation of HNF 4α. Treatment with different concentrations (1-10.8 µM) of NHDC for various periods (0-72 h) inhibited liver cancer cells (HepG2, Hep3B) growth as well as colony formation followed by induction of apoptosis in a concentration dependent manner. NHDC also induced expression of the apoptosis regulating genes as well as inhibiting the action of STAT3. These inhibitory effects were associated with enhancement of expression and DNA binding activity of HNF 4α. In vivo study confirmed that liver tumor growth was prevented with NHDC (5 mg/kg), and its effect was also related with inhibition of STAT3 pathway through enhancement of expression and DNA binding activity of HNF 4α. Moreover, siRNA of HNF 4α abolished NHDC-induced cell growth inhibition as well as DNA binding activity and phosphorylation of STAT3. Pull down assay docking prediction analysis proved that NHDC directly binds to hydrophobic fatty acid ligand binding site of HNF 4α. A novel naphthofuran compound, NHDC inhibited liver tumor growth by inactivating of STAT3 through direct biding to HNF 4α. © 2015 Wiley Periodicals, Inc. © 2015 Wiley Periodicals, Inc.
    Molecular Carcinogenesis 04/2015; DOI:10.1002/mc.22311 · 4.77 Impact Factor
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    ABSTRACT: Melanoma is the most aggressive skin cancer and its incidence is gradually increasing worldwide. Patients with metastatic melanoma have a very poor prognosis (estimated 5-year survival rate of <16%). In the last few years, several drugs have been approved for malignant melanoma, such as tyrosine kinase inhibitors and immune checkpoint blockades. Although new therapeutic agents have improved progression-free and overall survival, their use is limited by drug resistance and drug-related toxicity. At the same time, adoptive cell therapy of metastatic melanoma with tumor-infiltrating lymphocytes has shown promising results in preclinical and clinical studies. In this review, we summarize the currently available drugs for treatment of malignant melanoma. In addition, we suggest cytokine-induced killer (CIK) cells as another candidate approach for adoptive cell therapy of melanoma. Our preclinical study and several previous studies have shown that CIK cells have potent anti-tumor activity against melanomas in vitro and in an in vivo human tumor xenograft model without any toxicity.
    Immune Network 04/2015; 15(2):58-65. DOI:10.4110/in.2015.15.2.58
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    ABSTRACT: Two active substances from ginseng fermented using Ganoderma lucidum mycelia were investigated for antiproliferative effects against the human lung cancer cell line A549. The chloroform fraction of fermented ginseng extracts showed a strong antiproliferative effect. This fraction was isolated and purified using silica gel and C18 resin column chromatography and semi-preparative reverse phase HPLC. The structures of isolated compounds were determined using spectroscopic methods (ESI-MS, 1H and 13C NMR). Isolated compounds were identified as ginsenoside compound K and 3-oxo-compound K. Both inhibited A549 cell growth in a dose-dependent manner. Cell viability values for ginsenoside compound K were 74.88, 59.30, 5.76, 5.79, and 6.27% at 6.25, 12.50, 25.00, 50.00, and 100.00 μg/mL, respectively, and ginsenoside 3-oxo-compound K showed values 89.40, 59.62, 6.05, and 4.64% at 3.70, 7.50, 15.00, and 30.00 μg/mL, respectively. Compound K and 3-oxo-compound K from fermented ginseng can be used as natural anti-cancer agents.
    Food science and biotechnology 04/2015; 24(2):567-574. DOI:10.1007/s10068-015-0074-3 · 0.66 Impact Factor
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    ABSTRACT: Activation of nuclear factor kappa-B (NF-κB) is implicated in drug resistant of lung cancer cells. Our previous data showed that thiacremonone inhibited activation of NF-κB. In the present study, we investigated whether thiacremonone enhanced susceptibility of lung cancer cells to a common anti-cancer drug paclitaxel by further inhibition of NF-κB. Thus, we used the threefold lower doses of IC50 values (50 μg/ml thiacremonone and 2.5 nM paclitaxel). We found that combination treatment with thiacremonone and paclitaxel was more susceptible (combination index; 0.40 in NCI-H460 cells and 0.46 in A549 cells) in cell growth inhibition of two types of lung cancer cell lines compared to a single agent treatment. Consistent with the combination effect on cancer cell growth inhibition, the combination treatment further induced apoptotic cell death and arrested the cancer cells in G2/M phase accompanied with a much lower expression of cdc2 and cyclin B1, and inhibited colony formation. Much more inactivation of NF-κB and greater expression of NF-κB target apoptosis regulated genes such as caspase-8 and PARPs were found by the combination treatment. Molecular model and pull down assay as well as MALDI-TOF analysis demonstrated that thiacremonone directly binds to p50. These data indicated that thiacremonone leads to increased apoptotic cell death in lung cancer cell lines through greater inhibition of NF-κB by the combination treatment with paclitaxel.
    Archives of Pharmacal Research 03/2015; DOI:10.1007/s12272-015-0589-4 · 1.75 Impact Factor
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    ABSTRACT: Saururus chinensis is a medicinal plant used to treat jaundice, pneumonia, edema, fever, and several inflammatory diseases. Saucerneol D (SD), a lignan constituent of this plant, has antioxidant, anti-asthmatic, and anti-inflammatory activities. SD has been previously reported to inhibit the pro-inflammatory responses of RAW264.7 cells and primary mast cells. In this study, we investigated the effect of SD on the functions of dendritic cells (DCs). SD was isolated from methanol extract of the roots of S. chinensis. Bone marrow-derived DCs were used as target cells. The effects of SD on the following DC functions were examined: surface molecule expression, cytokine expression, migration, allogenic T cell activation, heme oxygenase-1 expression, and Toll-like receptor 4 signaling. In lipopolysaccharide (LPS)-treated DCs, SD inhibited the expression of cell surface molecules (MHC I/II, CD40, CD80, and CD86), the production of inflammatory mediators (nitric oxide, IL-12, IL-1β, and TNF-α), and allogenic T cell activation capacity. SD also inhibited DC migration toward MIP-3β by down-regulating CCR7 expression. SD attenuated LPS-induced activation of NF-κB and MAPK signaling in DCs, but did not directly inhibit kinase activities of IRAK1, IRAK4, TAK1, or IKKβ in enzymatic assays. SD did not inhibit LPS binding to myeloid differentiation protein-2, co-receptor of TLR4. SD increased the production of reactive oxygen species, Nrf-2, and heme oxygenase (HO)-1, which degrades the heme to immunosuppressive carbon monoxide and biliverdin, which may underlie the anti-inflammatory effects in SD-treated DCs. Taken together, these data suggest that SD suppresses LPS-induced activation of DCs through the induction of HO-1, but not by directly affecting Toll-like receptor 4 signaling. Copyright © 2015. Published by Elsevier Ireland Ltd.
    Journal of ethnopharmacology 03/2015; 166. DOI:10.1016/j.jep.2015.03.020 · 2.94 Impact Factor
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    ABSTRACT: Background and purpose cAMP as a second messenger stimulates expression of microphthalmia-associated transcription factor (MITF) or tyrosinase gene under ultraviolet B (UVB)-induced skin pigmentation. Diphenylmethylene hydrazinecarbothioamide (QNT 3-80) inhibits α-melanocyte-stimulating hormone (α-MSH)-induced melanin production in B16 murine melanoma cells but its molecular basis remains to be defined. Here, we investigated an antimelanogenic mechanism of QNT 3-80 in the amelioration of skin hyperpigmentation. Experimental approach cAMP-elevated melanocyte cultures were used for in vitro assays and UVB-irradiated dorsal skins of guinea pigs for in vivo pigmentation. Immunoprecipitation, kemptide phosphorylation, fluorescence analysis and docking simulation were applied to elucidate a molecular mechanism of QNT 3-80. Key results QNT 3-80 inhibited melanin production in vitro under cAMP-elevated melanocyte cultures including those from human foreskins, and also ameliorated hyperpigmentation in vivo under UVB-irradiated dorsal skins of guinea pigs. As a mechanism, QNT 3-80 directly antagonized cAMP binding to the regulatory subunit of protein kinase A (PKA), nullified the dissociation and activation of inactive PKA holoenzyme in melanocytes, and fitted into the cAMP-binding site on the crystal structure of human PKA under the most energetically favorable simulation. QNT 3-80 consequently inhibited cAMP- or UVB-induced phosphorylation (activation) of cAMP-responsive element (CRE)-binding protein (CREB) in vitro and in vivo, thus down-regulating expression of MITF or tyrosinase gene in the melanogenic process. Conclusions and Implications Taken together, this study suggests a significant implication of QNT 3-80 in the treatment of skin disorders with hyperpigmented patches via the cAMP-binding site of PKA as a molecular target. This article is protected by copyright. All rights reserved.
    British Journal of Pharmacology 03/2015; DOI:10.1111/bph.13134 · 4.99 Impact Factor
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    ABSTRACT: Two new iridoids, 6-O-[(E)-feruloyl]jioglutin D (1) and 6-O-(4-hydroxybenzoyl)jioglutin D (2), and six known compounds, minecoside (3), specioside (4), picroside II (5), picroside III (6), 4-hydroxybenzoic acid (7), and martynoside (8), were isolated from the stem of Catalpa ovata. The structures of the new compounds were established on the basis of spectroscopic techniques, including 1D- and 2D-NMR.
    Helvetica Chimica Acta 03/2015; 98(3). DOI:10.1002/hlca.201400203 · 1.39 Impact Factor
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    ABSTRACT: The aim of this study was to investigate the involvement of dopaminergic receptors (DR) in behavioral sensitization, as measured by locomotor activity, and the over-expression of cocaine- and amphetamine-regulated transcript (CART) peptides after repeated administration of cocaine in mice. Repeated administrations of cocaine induced behavioral sensitization and CART over-expression in mice. The levels of striatal CART mRNA were significantly increased on the 3(rd) day. CART peptides were over-expressed on the 5(th) day in the striata of behaviorally sensitized mice. A higher proportion of CART(+) cells in the cocaine-treated mice were present in the nucleus accumbens (NAc) shell than in the dorsolateral (DL) part of caudate putamen (CP). The concomitant administration of both D1R and D2R antagonists, SCH 23390 (D1R selective) and raclopride (D2R selective), blocked cocaine induced-behavioral sensitization, CART over-expression, and cyclic adenosine 5'-monophosphate (cAMP)/protein kinase A (PKA)/phospho-cAMP response element-binding protein (pCREB) signal pathways. SCH 23390 more predominantly inhibited the locomotor activity, CART over-expression, pCREB and PKA activity than raclopride. Cocaine induced-behavioral sensitization was also attenuated in the both D1R and D2R knockout (KO) mice, respectively. CART over-expression and activated cAMP/PKA/pCREB signal pathways were inhibited in the D1R-KO mice, but not in the D2R-KO mice. It is suggested that behavioral sensitization, CART over-expression and activated cAMP/PKA/pCREB signal pathways induced by repeated administration of cocaine could be more predominantly mediated by D1R.
    Korean Journal of Physiology and Pharmacology 03/2015; 19(2):89-97. DOI:10.4196/kjpp.2015.19.2.89 · 1.26 Impact Factor
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    ABSTRACT: Objective Chronic excessive food intake leads to energy imbalance, resulting in hepatic steatosis and inflammation. Interleukin-32 (IL-32) is known to be a pro-inflammatory cytokine associated with chronic inflammation and cancer. Therefore, the relationship between IL-32 and chronic excessive food intake-induced liver disease was investigated.Methods Male IL-32β transgenic and wild-type mice were fed a high-fat diet (HFD) for 15 weeks. They were compared with wild-type mice on a standard chow diet. Daily food intake, body and liver weight, serum biochemistry, histopathological analysis of the liver, and hepatic immune response were determined.ResultsIL-32β mice on HFD showed lower lipid accumulation, reduced infiltration of immune cells, and lower production of pro-inflammatory cytokines in the liver. The expression of the peroxisome proliferator-activated receptor γ (PPARγ) was downregulated and the adenosine 50-monophosphate (AMP)-activated protein kinase (AMPK) was activated in the liver of IL-32β mice compared to wild-type mice. Furthermore, IL-32β over-expression activated the AMPK pathway and IL-32β downregulation inactivated the AMPK pathway in HepG2 cells under high-glucose conditions.Conclusions These data suggest that IL-32β modulates lipid accumulation through inhibition of PPARγ expression and AMPK activation.
    Obesity 02/2015; 23(3). DOI:10.1002/oby.21001 · 4.39 Impact Factor
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    ABSTRACT: Leptin, a hormone mainly produced from adipose tissue, has been shown to induce proliferation of cancer cells. However, the molecular mechanisms underlying leptin-induced tumor progression have not been clearly elucidated. In the present study, we investigated the role of autophagy in leptin-induced cancer cell proliferation using human hepatoma (HepG2) and breast cancer cells (MCF-7), and tumor growth in a xenograft model. Herein, we showed that leptin treatment caused autophagy induction as assessed by increase in expression of autophagy-related genes, including beclin-1, Atg5 and LC3 II, further induction of autophagosome formation and autophagic flux. Interestingly, inhibition of autophagic process by treatment with inhibitors and LC3B gene silencing blocked leptin-induced increase in cell number and suppression of apoptosis, indicating a crucial role of autophagy in leptin-induced tumor progression. Moreover, gene silencing of p53 or FoxO3A prevented leptin-induced LC3 II protein expression, suggesting an involvement of p53/FoxO3A axis in leptin-induced autophagy activation. Leptin administration also accelerated tumor growth in BALB/c nude mice, which was found to be autophagy dependent. Taken together, our results demonstrate that leptin-induced tumor growth is mediated by autophagy induction and autophagic process would be a promising target to regulate development of cancer caused by leptin production.
    Oncotarget 01/2015; · 6.63 Impact Factor
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    ABSTRACT: H9, a novel herbal extract, demonstrated cytotoxicity in A549 non-small cell lung cancer (NSCLC) cell lines. In this study, we investigated whether H9, and/or co-treatment with an anticancer drug, pemetrexed (PEM), inhibited tumor growth in BALB/c nude mice models bearing A549 NSCLC cells. The mice were separated into groups and administered H9 and PEM for 2 weeks. Protein and mRNA levels were detected using western blotting and reverse transcription polymerase chain reaction (RT-PCR), respectively; immuno histochemistry (IHC) was also performed on the tumor tissues. H9 and co-treatment with PEM induced cleavages of pro-apoptotic factors, such as caspase-3, caspase-8, caspase-9, and poly ADP-ribose polymerase (PARP). Expression levels of cell-death receptors involving Fas/FasL, TNF-related apoptosis-inducing ligands (TRAIL), and TRAIL receptors were increased by H9 and co-treatment with PEM. Furthermore, analysis of levels of cell-cycle modulating proteins indicated that tumor cells were arrested in G1/S phase. In addition, phosphatidylinositol-4, 5-bisphosphate 3-kinase (PI3K)/Akt survival signaling pathways were inhibited by H9 and co-treatment with PEM. In conclusion, H9 and co-treatment with PEM inhibited tumor growth in BALB/c nude mice models bearing A549 NSCLC cells. These results indicate that H9 and co-treatment with PEM can be used as an anticancer therapy in NSCLC.
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    ABSTRACT: We studied whether bee venom (BV) inhibits cervical tumor growth through enhancement of death receptor (DR) expressions and inactivation of nuclear factor kappa B (NF-κB) in mice. In vivo study showed that BV (1 mg/kg) inhibited tumor growth. Similar inhibitory effects of BV on cancer growth in primary human cervical cancer cells were also found. BV (1-5 μg/ml) also inhibited the growth of cancer cells, Ca Ski and C33Aby the induction of apoptotic cell death in a dose dependent manner. Agreed with cancer cell growth inhibition, expression of death receptors; FAS, DR3 and DR6, and DR downstream pro-apoptotic proteins including caspase-3 and Bax was concomitantly increased, but the NF-κB activity and the expression of Bcl-2 were inhibited by treatment with BV in tumor mice, human cancer cell and human tumor samples as well as cultured cancer cells. In addition, deletion of FAS, DR3 and DR6 by small interfering RNA significantly reversed BV-induced cell growth inhibitory effects as well as NF-κB inactivation. These results suggest that BV inhibits cervical tumor growth through enhancement of FAS, DR3 and DR6 expression via inhibition of NF-κB pathway.
    Oncotarget 01/2015; · 6.63 Impact Factor
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    ABSTRACT: Alcohol abuse and alcoholism lead to alcoholic liver disease, which is a major type of chronic liver disease worldwide. Interleukin-32 (IL-32) is a novel cytokine involved in inflammation and cancer development. However, the role of IL-32 in chronic liver disease has not been reported. Here, we tested the effect of IL-32γ on ethanol-induced liver injury in IL-32γ-overexpressing transgenic mice (IL-32γ mice) after chronic ethanol feeding. Male C57BL/6 and IL-32γ mice (10-12 weeks old) were fed a Lieber-DeCarli diet containing 6.6% ethanol for 6 weeks. IL-32γ-transfected HepG2 and Huh7 cells as well as primary hepatocytes from IL-32γ mice were treated with or without ethanol.The hepatic steatosis and damage induced by ethanol administration were attenuated in IL-32γ mice. Ethanol-induced Cytochrome P450 2E1 expression and hydrogen peroxide levels were decreased in the livers of IL-32γ mice, primary hepatocytes from IL-32γ mice and IL-32γ-overexpressing human hepatic cells. The ethanol-induced expression levels of cyclooxyganase-2 and interleukin-6 were reduced in the livers of IL-32γ mice. Because nuclear transcription factor kappa B (NF-κB) is a key redox transcription factor of inflammatory response, we examined NF-κB activity. Ethanol-induced NF-κB activities were significantly lower in the livers of IL-32γ mice than in wild-type mice. Furthermore, reduced infiltration of natural killer cells, cytotoxic T cells, and macrophages in the liver after ethanol administration was observed in the livers of IL-32γ mice. These data suggest that IL-32γ prevents ethanol-induced hepatic injury via the inhibition of oxidative damage and inflammatory responses.
    Clinical Science 01/2015; DOI:10.1042/CS20140576 · 5.63 Impact Factor
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    ABSTRACT: PRDX6 is a bifunctional protein with both glutathione peroxidase (GPx) and iPLA2 activities. Even though several pathophysiological functions have been studied, the definitive role of PRDX6 on tumor growth has been not clear. Here, we compared carcinogen-induced tumor growth in PRDX6 transgenic (Tg) mice and non Tg mice to evaluate roles of PRDX6 in lung tumor development. Urethane (1g/kg)-induced tumor incidence in PRDX6 Tg mice was significant higher compared to non Tg mice. In the tumors of PRDX6 Tg mice, the activation of JAK2/STAT3 and STAT3 DNA binding were also increased, which is accompanied with increased GPx and iPLA2 activities. PRDX6 was colocalized with JAK2 in tumor tissues and lung cancer cells, and also showed physical interaction with JAK2. We found that the increasing level of Prdx6 increases the activation of the JAK2/STAT3 pathway. Furthermore, PRDX6 Tg mice showed altered cytokine levels in the tumors, especially leading to increased CCL5 level. We validated that the activation of JAK2 was also decreased in lung tumors of CCR5(-/-) mice, and CCL5 increased the JAK2/STAT3 pathway in the lung cancer cells. Thus, our findings suggest that PRDX6 promotes lung tumor development via its mediated and CCL5 associated activation of the JAK2/STAT3 pathways. Copyright © 2015. Published by Elsevier Inc.
    Free Radical Biology and Medicine 01/2015; 80. DOI:10.1016/j.freeradbiomed.2014.12.022 · 5.71 Impact Factor
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    ABSTRACT: This experiment was designed to investigate whether 4-O-methylhonokiol (MH), a principal ingredient of Magnolia (M.) officinalis bark, alleviated acute intraperitoneal (i.p.) kainic acid- (KA-) induced brain blood barrier dysfunction (BBBD) via pathological examination and cytological analyses of the brain tissues of mice. KA (10-30 mg/kg) time- and dose-dependently increased the water content of brain tissues and induced edema and encephalopathy. However, pretreatment with MH (5 and 20 mg/kg, i.p.) significantly reduced the water content of the brain compared to that observed in the KA control group. Furthermore, MH significantly and dose-dependently reversed the remarkable variations in evan's blue dye (EBD) staining and malondialdehyde (MDA) levels that were induced by KA (10 mg/kg, i.p.). MH also decreased the elevated seizure scores that were induced by KA (10 mg/kg, i.p.) in mice in a manner similar to scavengers such as DMTU and trolox. Additionally, MH significantly scavenged intracellular ROS and Ca(2+) within hippocampal cells. The tight junction seals mediated by claudin (Cld-5) were also found to be modulated by MH. MH efficiently reduced 1,1-diphenyl-2-picrylhydrazyl (DPPH) (IC50, 52.4 mM) and (•)OH with an electron spin resonance (ESR) signal rate constant of 4 × 10(9) M(-1) · S(-1), which is close to the reactivity of the vitamin E analog trolox. Taken together, these results suggest that MH may enhance radical scavenging in lipid and hydrophobic environments, which may be important for the physiological activity of the barrier.
    BioMed Research International 01/2015; 2015:893163. DOI:10.1155/2015/893163 · 2.71 Impact Factor
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    ABSTRACT: The activity-guided fractionation of the MeOH extract of the flower of Paulownia coreana led to the isolation of a new geranylated flavanone, 3'-O-methyl-5'-hydroxydiplacol (1), along with 10 known compounds (2-11). Their structures were determined using spectroscopic techniques, which included one and two dimensional (1- and 2D)-NMR. Among the isolates, compounds 1-6 showed potent inhibitory activities against lipopolysaccharide (LPS)-induced nitric oxide production with IC50 values ranging 1.48 to 16.66 µM.
    Chemical & pharmaceutical bulletin 01/2015; 63(5):384-7. DOI:10.1248/cpb.c14-00839 · 1.38 Impact Factor

Publication Stats

4k Citations
886.91 Total Impact Points

Institutions

  • 2015
    • Chonnam National University
      • School of Dentistry
      Gwangju, Gwangju, South Korea
  • 2002–2015
    • Chungbuk National University
      • College of Pharmacy
      Chinsen, Chungcheongbuk-do, South Korea
  • 2006–2012
    • Konkuk University
      • • Department of Bioscience and Technology
      • • Bio/Molecular Informatics Center
      Sŏul, Seoul, South Korea
  • 1998–2011
    • Korea Food and Drug Administration
      Seishō-gun, North Gyeongsang, South Korea
  • 2008
    • Safety Research Institute
      Georgia, United States
  • 2003
    • Korea Research Institute of Bioscience and Biotechnology KRIBB
      • Laboratory of Cellular Biology
      Ansan, Gyeonggi, South Korea