Jin Tae Hong

Chonnam National University, Gwangju, Gwangju, South Korea

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Publications (336)979.7 Total impact

  • Oncotarget 09/2015; 6(29):26716-26728. DOI:10.18632/oncotarget.5777 · 6.36 Impact Factor
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    ABSTRACT: A concise and expeditious approach to the total synthesis of broussonone A, a p-quinol natural compound, has been developed. The key features of the synthesis include the Grubbs II catalyst mediated cross metathesis of two aromatic subunits, and a chemoselective oxidative dearomatizationin the presence of two phenol moieties. Especially, optimization associated with the CM reaction of ortho-alkoxystyrenes was also studied, which are known to be ineffective for Ru-catalyzed metathesis reactions under conventional reaction conditions because ortho-alkoxy group could coordinate to the ruthenium center, resulting in the potential complication of catalyst inhibition.
    Molecules 09/2015; 20(9):15966-75. DOI:10.3390/molecules200915966 · 2.42 Impact Factor
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    ABSTRACT: Three new neo-clerodane diterpenoids (1-3) along with 12 known compounds (4-15) were isolated from a methanol extract of the aerial parts of Scutellaria barbata. The structures of 1-3 were determined by interpretation of their 1D and 2D NMR spectroscopic data as well as HRESIMS values. All isolated compounds were tested for their inhibitory effects on LPS-induced nitric oxide production in RAW 264.7 macrophages. Compounds 1-4, 7, and 10-12 were found to inhibit nitric oxide production with IC50 values ranging from 20.2 to 35.6 μM.
    Journal of Natural Products 09/2015; 78(9). DOI:10.1021/acs.jnatprod.5b00126 · 3.80 Impact Factor
  • Qinghao Jin · Chul Lee · Jin Woo Lee · Dongho Lee · Youngsoo Kim · Jin Tae Hong · Jin Sook Kim · Joo-Hwan Kim · Mi Kyeong Lee · Bang Yeon Hwang
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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 09/2015; 63(5):384-7. DOI:10.1248/cpb.c14-00839 · 1.16 Impact Factor
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    ABSTRACT: Alzheimer's disease (AD) is the most common form of dementia. It is characterized by beta-amyloid (Aβ) peptide fibrils, which are extracellular depositions of a specific protein, and is accompanied by extensive neuroinflammation. Various studies have demonstrated risk factors that can affect AD pathogenesis, and they include accumulation of Aβ, hyperphosphorylation of tau protein, and neuroinflammation. Among these detrimental factors, neuroinflammation has been highlighted by epidemiologic studies suggesting that use of anti-inflammatory drugs could significantly reduce the incidence of AD. Evidence suggests that astrocytes, microglia, and infiltrating immune cells from periphery might contribute to or modify the process of neuroinflammation and neurodegeneration in AD brains. In addition, recent data indicate that microRNAs may affect neuroinflammatory responses in the brain. This article focuses on supportive evidence that neuroinflammation plays a critical role in AD development. In addition, we depict putative therapeutic capacity of anti-inflammatory drugs for AD prevention or treatment. We also discuss pathogenic mechanisms by which astrocytes, microglia, T cells and microRNA participate in AD and the neuroprotective mechanisms of anti-inflammatory drugs.
    Archives of Pharmacal Research 08/2015; DOI:10.1007/s12272-015-0648-x · 2.05 Impact Factor
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    ABSTRACT: Multiple sclerosis (MS) is a complex disease with an unknown etiology and has no effective medications despite extensive research. Antioxidants suppress oxidative damages which are implicated in the pathogenesis of MS. In this study, we showed that the expression of an antioxidant protein peroxiredoxin 6 (PRDX6) is markedly increased in spinal cord of mice with experimental autoimmune encephalomyelitis (EAE) compared to other PRDXs. PRDX6 transgenic (Tg) mice displayed a significant decrease in clinical severity and attenuated demyelination in EAE compared to wide type mice. The increased PRDX6 expression in astrocytes of EAE mice and MS patients reduced MMP9 expression, fibrinogen leakage, chemokines, and free radical stress, leading to reduction in blood-brain-barrier (BBB) disruption, peripheral immune cell infiltration, and neuroinflammation. Together, these findings suggest that PRDX6 expression may represent a therapeutic way to restrict inflammation in the central nervous system and potentiate oligodendrocyte survival, and suggest a new molecule for neuroprotective therapies in MS.
    Oncotarget 08/2015; 6(25):20875-84. DOI:10.18632/oncotarget.5205 · 6.36 Impact Factor
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    ABSTRACT: Angiogenesis is the process of new vessel formation from pre-existing blood vasculature and is critical for continuous tumor growth. We previously reported that an ethanolic extract of Gleditsia sinensis thorns (EEGS) and its active constituent, cytochalasin H, have anti-angiogenic activity in vitro and in vivo via suppression of endothelial cell functions. In the present study, EEGS and cytochalasin H were observed to efficiently inhibit tumor growth in an in ovo xenograft model without significant toxicity. We repeatedly observed the anti-tumor and anti-metastatic effects of EEGS in representative animal models. These results suggest that EEGS and its active constituent, cytochalasin H, are potential candidates for the development of anti-angiogenic cancer drugs.
    Biological & Pharmaceutical Bulletin 07/2015; 38(6):909-12. DOI:10.1248/bpb.b14-00647 · 1.83 Impact Factor
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    ABSTRACT: Peroxiredoxin 6 (Prdx6) plays important and complex roles in the process of inflammation, but its role in the development of rheumatoid arthritis (RA) remains unclear. Thus, we investigated the roles and mechanisms of Prdx6 in the development of arthritis in Collagen antibody-induced arthritis (CAIA) and antibody-induced arthritis (AIA) induced Prdx6 overexpressed transgenic mice as well as Prdx6 transfected RAW 264.7 cells, and macrophage isolated Prdx6 overexpressed transgenic mice and synoviocytes. Arthritis developments were induced with CAIA or AIA methods. Prdx6 transfected RAW 264.7 cells, and macrophage isolated Prdx6 overexpressed transgenic mice and synoviocytes were used for pro-inflammation responses and mechanisms. Clinical score, histopathological changes, NO generation, iNOS and COX2 expression, and NF-κB and AP-1 activities were determined in cultured macrophage and synoviocytes as well as joint tissues of mice by Western bloting, gel electromobility shift assay and histochemistry analysis. CAIA and AIA-induced arthritis development and pro-inflammation response were more exacerbated in Prdx6 overexpressed transgenic mice as well as Prdx6 transfected RAW264.7 cells, and macrophage isolated Prdx6 overexpressed transgenic mice and synoviocytes accompanied with up-regulation of JNK pathway. Moreover, JNK inhibitor completely blocked RA development and pro-inflammation responses. Our findings suggest that overexpression of Prdx6 might promote development of RA through activation of NF-κB/AP-1 coupled JNK pathway. This article is protected by copyright. All rights reserved. © 2015, American College of Rheumatology.
    Arthritis and Rheumatology 07/2015; DOI:10.1002/art.39284
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    ABSTRACT: To characterize the changes in global gene expression in the distal colon of constipated SD rats in response to the laxative effects of aqueous extracts of Liriope platyphylla (AEtLP), including isoflavone, saponin, oligosaccharide, succinic acid and hydroxyproline, the total RNA extracted from the distal colon of AEtLP-treated constipation rats was hybridized to oligonucleotide microarrays. The AEtLP treated rats showed an increase in the number of stools, mucosa thickness, flat luminal surface thickness, mucin secretion, and crypt number. Overall, compared to the controls, 581 genes were up-regulated and 216 genes were down-regulated by the constipation induced by loperamide in the constipated rats. After the AEtLP treatment, 67 genes were up-regulated and 421 genes were down-regulated. Among the transcripts up-regulated by constipation, 89 were significantly down-regulated and 22 were recovered to the normal levels by the AEtLP treatment. The major genes in the down-regulated categories included Slc9a5, klk10, Fgf15, and Alpi, whereas the major genes in the recovered categories were Cyp2b2, Ace, G6pc, and Setbp1. On the other hand, after the AEtLP treatment, ten of these genes down-regulated by constipation were up-regulated significantly and five were recovered to the normal levels. The major genes in the up-regulated categories included Serpina3n, Lcn2 and Slc5a8, whereas the major genes in the recovered categories were Tmem45a, Rerg and Rgc32. These results indicate that several gene functional groups and individual genes as constipation biomarkers respond to an AEtLP treatment in constipated model rats.
    PLoS ONE 07/2015; 10(7):e0129664. DOI:10.1371/journal.pone.0129664 · 3.23 Impact Factor
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    ABSTRACT: Flavonoids are a diverse family of natural phenolic compounds commonly found in fruits and vegetables. Epidemiologic studies showed that flavonoids also reduce the risk of colon cancer. Tectochrysin is one of the major flavonoids of Alpinia oxyphylla Miquel. However, the anti-cancer effects and the molecular mechanisms of tectochrysin in colon cancer cells have not yet been reported. We investigated whether tectochrysin could inhibit colon cancer cell growth at 1, 5, 10 μg/ml. In in vivo study, we injected a tectochrysin treatment dose of 5 mg/kg to each mouse. Tectochrysin suppressed the growth of SW480 and HCT116 human colon cancer cells. The expression of DR3, DR4 and Fas were significantly increased, and pro-apoptotic proteins were also increased. Tectochrysin treatment also inhibited activity of NF-κB. A docking model indicated that tectochrysin binds directly to the p50 unit. In in vivo, tumor weights and volumes in mice were reduced when treated with tectochrysin. Tectochrysin leads to apoptotic cell death in colon cancer cells through activation of death receptors expression via the inhibition of NF-κB. Tectochrysin can be a useful agent for the treatment of colon cancer cell growth as well as an adjuvant agent for chemo-resistant cancer cells growth.
    Molecular Cancer 06/2015; 14(1):124. DOI:10.1186/s12943-015-0377-2 · 4.26 Impact Factor
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    ABSTRACT: Accumulation of beta-amyloid and neuroinflammation trigger Alzheimer's disease. We previously found that lipopolysaccharide (LPS) caused neuroinflammation with concomitant accumulation of beta-amyloid peptides leading to memory loss. A variety of anti-inflammatory compounds inhibiting nuclear factor kappaB (NF-κB) activation have showed efficacy to hinder neuroinflammation and amyloidogenesis. We also found that bee venom (BV) inhibits NF-κB. A mouse model of LPS-induced memory loss used administration of BV (0.8 and 1.6 μg/kg/day, i.p.) to ICR mice for 7 days before injection of LPS (2.5 mg/kg/day, i.p.). Memory loss was assessed using a Morris water maze test and passive avoidance test. For in vitro study, we treated BV (0.5, 1, and 2 μg/mL) to astrocytes and microglial BV-2 cells with LPS (1 μg/mL). We found that BV inhibited LPS-induced memory loss determined by behavioral tests as well as cell death. BV also inhibited LPS-induced increases in the level of beta-amyloid (Aβ), β-and γ-secretases activities, NF-κB and its DNA-binding activity and expression of APP, and BACE1 and neuroinflammation proteins (COX-2, iNOS, GFAP and IBA-1) in the brain and cultured cells. In addition, pull-down assay and molecular modeling showed that BV binds to NF-κB. BV attenuates LPS-induced amyloidogenesis, neuroinflammation, and therefore memory loss via inhibiting NF-κB signaling pathway. Thus, BV could be useful for treatment of Alzheimer's disease.
    Journal of Neuroinflammation 06/2015; 12(1):124. DOI:10.1186/s12974-015-0344-2 · 5.41 Impact Factor
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    ABSTRACT: Tyrosinase inhibitors are an important component of cosmetic products. Our previous studies have proposed that eck-ol isolated from the brown alga Ecklonia cava, can be explored as a tyrosinase inhibitor. However, cellular activities and mechanism of action of eckol remain unknown. Therefore, the current study analyzed the eckol binding modes using the crystal structure of Bacillus megaterium tyrosinase. The effects of eckol on melanin synthesis induced by α-melanocyte stimulating hormone in B16F10 melanoma cells were also investigated. We predicted the 3D structure of tyrosinase and used a docking algorithm to simulate binding between tyrosinase and eckol. These molecular modeling studies were successful (calculated binding energy value, -115.84 kcal mol-1) and indicated that eckol interacts with Asn205, His208, and Arg209. Furthermore, eckol markedly inhibited tyrosinase activity and melanin synthesis in B16F10 melanoma cells. We also found that eckol decreased the expression of tyrosinase, tyrosinase-related protein (TRP) 1, and TRP2. These results indicate that eckol is a potent inhibitor of melanogenesis, and this fnding may be useful for the development of novel pharmaceutical and cosmetic agents.
    06/2015; 30(2):163-170. DOI:10.4490/algae.2015.30.2.163
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    ABSTRACT: C-C chemokine receptor 5 (CCR5) regulates leukocyte chemotaxis and activation, and its deficiency exacerbates development of nephritis. Therefore, we investigated the role of CCR5 during lipopolysaccharide (LPS)-induced acute kidney injury. CCR5-deficient (CCR5-/-) and wild-type (CCR5+/+) mice, both aged about 10 months, had acute renal injury induced by intraperitoneal injection of LPS (10 mg/kg). Compared with CCR5+/+ mice, CCR5-/- mice showed increased mortality and renal injury, including elevated creatinine and blood urea nitrogen levels, following LPS challenge. Compared to CCR5+/+ mice, CCR5-/- mice also exhibited greater increases in the serum concentrations of pro-inflammatory cytokines, including tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-1β following LPS challenge. Furthermore, infiltration of macrophages and neutrophils, expression of intracellular adhesion molecule (ICAM)-1, and the number of apoptotic cells were more greatly increased by LPS treatment in CCR5-/- mice than in CCR5+/+ mice. The concentrations of pro-inflammatory cytokines such as TNF-α, IL-6, and IL-1β were also significantly increased in the kidney of CCR5-/- mice after LPS challenge. Moreover, primary kidney cells from CCR5-/- mice showed greater increases in TNF-α production and p38 MAP kinase activation following treatment with LPS compared with that observed in the cells from CCR5+/+ mice. LPS-induced TNF-α production and apoptosis in the primary kidney cells from CCR5-/- mice were inhibited by treatment with p38 MAP kinase inhibitor. These results suggest that CCR5 deficiency increased the production of TNF-α following LPS treatment through increased activation of the p38 pathway in the kidney, resulting in renal apoptosis and leukocyte infiltration and led to exacerbation of LPS-induced acute kidney injury.
    Archives of Toxicology 06/2015; DOI:10.1007/s00204-015-1530-9 · 5.98 Impact Factor
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    ABSTRACT: Snake venom toxin (SVT) from Vipera lebetina turanica contains a mixture of different enzymes and proteins. Peroxiredoxin 6 (PRDX6) is known to be a stimulator of lung cancer cell growth. PRDX6 is a member of peroxidases, and has calcium-independent phospholipase A2 (iPLA2) activities. PRDX6 has an AP-1 binding site in its promoter region of the gene. Since AP-1 is implicated in tumor growth and PRDX6 expression, in the present study, we investigated whether SVT inhibits PRDX6, thereby preventing human lung cancer cell growth (A549 and NCI-H460) through inactivation of AP-1. A docking model study and pull down assay showed that SVT completely fits on the basic leucine zipper (bZIP) region of c-Fos of AP-1. SVT (0-10 μg/ml) inhibited lung cancer cell growth in a concentration dependent manner through induction of apoptotic cell death accompanied by induction of cleaved caspase-3, -8, -9, Bax, p21 and p53, but decreased cIAP and Bcl2 expression via inactivation of AP-1. In an xenograft in vivo model, SVT (0.5 mg/kg and 1 mg/kg) also inhibited tumor growth accompanied with the reduction of PRDX6 expression, but increased expression of proapoptotic proteins. These data indicate that SVT inhibits tumor growth via inhibition of PRDX6 activity through interaction with its transcription factor AP-1.
    Oncotarget 06/2015; 6(26). DOI:10.18632/oncotarget.4192 · 6.36 Impact Factor
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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 · 5.14 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; 64. DOI:10.1016/j.biocel.2015.05.007 · 4.05 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 · 2.27 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(11). DOI:10.18632/oncotarget.3197 · 6.36 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 · 4.81 Impact Factor
  • Gwi Yeong Jang · Eun Mi Joung · Sang Hoon Lee · Jae-Hyun Jeong · Bang Yeon Hwang · Jin Tae Hong · Junsoo Lee · Heon Sang Jeong
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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 · 0.65 Impact Factor

Publication Stats

4k Citations
979.70 Total Impact Points


  • 2015
    • Chonnam National University
      • School of Dentistry
      Gwangju, Gwangju, South Korea
  • 2002–2015
    • Chungbuk National University
      • College of Pharmacy
      Chinsen, Chungcheongbuk-do, South Korea
  • 2010–2012
    • 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
  • 2006
    • Soonchunhyang University
      Onyang, Chungcheongnam-do, South Korea
  • 2003
    • Korea Research Institute of Bioscience and Biotechnology KRIBB
      • Laboratory of Cellular Biology
      Ansan, Gyeonggi, South Korea
    • Ewha Womans University
      Sŏul, Seoul, South Korea
  • 1993
    • Korea Institute of Toxicology
      Sŏul, Seoul, South Korea