Jin Tae Hong

Chonnam National University, Gwangju, Gwangju, South Korea

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Publications (344)1011.49 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Multiple sclerosis (MS), also known as disseminated sclerosis or encephalomyelitis disseminate, is an inflammatory disease in which myelin in the spinal cord and brain are damaged. IL-32α is known as a critical molecule in the pathophysiology of immune-mediated chronic inflammatory disease such as rheumatoid arthritis, chronic pulmonary disease, and cancers. However, the role of IL-32α on spinal cord injuries and demyelination is poorly understood. Recently, we reported that the release of proinflammatory cytokines were reduced in IL-32α-overexpressing transgenic mice. In this study, we investigated whether IL-32α plays a role on MS using experimental autoimmune encephalomyelitis (EAE), an experimental mouse model of MS, in human IL-32α Tg mice. The Tg mice were immunized with MOG35-55 suspended in CFA emulsion followed by pertussis toxin, and then EAE paralysis of mice was scored. We observed that the paralytic severity and neuropathology of EAE in IL-32α Tg mice were significantly decreased compared with that of non-Tg mice. The immune cells infiltration, astrocytes/microglials activation, and pro-inflammatory cytokines (IL-1β and IL-6) levels in spinal cord were suppressed in IL-32α Tg mice. Furthermore, NG2 and O4 were decreased in IL-32α Tg mice, indicating that spinal cord damaging was suppressed. In addition, in vitro assay also revealed that IL-32α has a preventive role against Con A stimulation which is evidenced by decrease in T cell proliferation and inflammatory cytokine levels in IL-32α overexpressed Jurkat cell. Taken together, our findings suggested that IL-32α may play a protective role in EAE by suppressing neuroinflammation in spinal cord.
    Oncotarget 11/2015; DOI:10.18632/oncotarget.6306 · 6.36 Impact Factor
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    ABSTRACT: Bee venom (BV) has been used as a traditional medicine to treat arthritis, rheumatism, back pain, cancerous tumors, and skin diseases. However, the effects of BV on the colon cancer and their action mechanisms have not been reported yet. We used cell viability assay and soft agar colony formation assay for testing cell viability, electro mobility shift assay for detecting DNA binding activity of nuclear factor kappa B (NF-κB) and Western blotting assay for detection of apoptosis regulatory proteins. We found that BV inhibited growth of colon cancer cells through induction of apoptosis. We also found that the expression of death receptor (DR) 4, DR5, p53, p21, Bax, cleaved caspase-3, cleaved caspase-8, and cleaved caspase-9 was increased by BV treatment in a dose dependent manner (0-5 μg/ml). Consistent with cancer cell growth inhibition, the DNA binding activity of nuclear factor kappa B (NF-κB) was also inhibited by BV treatment. Besides, we found that BV blocked NF-κB activation by directly binding to NF-κB p50 subunit. Moreover, combination treatment with BV and p50 siRNA or NF-κB inhibitor augmented BV-induced cell growth inhibition. However, p50 mutant plasmid (C62S) transfection partially abolished BV-induced cell growth inhibiton. In addition, BV significantly suppressed tumor growth in vivo. Therefore, these results suggested that BV could inhibit colon cancer cell growth, and these anti-proliferative effects may be related to the induction of apoptosis by activation of DR4 and DR5 and inhibition of NF-κB.
    Oncotarget 11/2015; DOI:10.18632/oncotarget.6295 · 6.36 Impact Factor
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    ABSTRACT: Nearly 7 to 10 million people are living with Alzheimer's disease (AD) worldwide. Senile plaques composed of β-amyloid (Aβ) are a pathological hallmark of Alzheimer's disease. Presenilin 2 (PS2) mutations increase Aβ generation in the brains of AD patients. The Aβ is generated through the sequential cleavage of amyloid precursor protein by β- and γ-secretases. Additionally, increasing evidences suggest that estrogen can reduce the development of AD via regulation of β-secretases activity and beta-site APP-cleaving enzyme (BACE1) expression. But the underlying correlation mechanism of Aβ generation byPS2mutations and estrogen remains to be clarified. To investigate the anti-amyloidogenesis effect of estrogen in a PS2 mutative condition, we examined memory impairment in ovariectomized PS2 mutation (N141I) mice in which cognitive function was assessed by the Morris water maze test and passive avoidance test. In addition, Western blot analysis, immunostaining, immunofluorescence staining, ELISA and enzyme activity assays were used to examine the degree of Aβ deposition in the brains. In the present study, Aβ accumulated more in the ovariectomized PS2 mutant mice brain, and greatly worsened memory impairment and glial activation as well as neurogenic inflammation. In parallel with increased memory impairment, activity of β-secretase and expression of the BACE1 increased inovariectomized PS2 mutant mice. Much higher activity of NF-κB was observed by EMSA in ovariectomized PS2 mutant mice. In addition, the Aβ level was decreased by treatment of β-estradiol through inhibiting BACE1 expression in PS2 transfacted PC12 cells. These results suggest that mutation of PS2 can lead to NF-κB mediate amyloidogensis, and this effect canbeamplified by the absence of estrogen.
    Brain Behavior and Immunity 11/2015; DOI:10.1016/j.bbi.2015.11.013 · 5.89 Impact Factor
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    ABSTRACT: Interleukin (IL)-32, mainly produced by T-lymphocytes, natural killer cells, epithelial cells, and blood monocytes, is dominantly known as a pro-inflammatory cytokine. However, the role of IL-32 on inflammatory disease has been doubtful according to diverse conflicting results. This study was designed to examine the role of IL-32β on the development of collagen antibody (CAIA) and lipopolysaccharide (LPS)-induced inflammatory arthritis. Our data showed that the paw swelling volume and clinical score were significantly reduced in the CAIA and LPS-treated IL-32β transgenic mice compared with non-transgenic mice. The populations of cytotoxic T, NK and dendritic cells was inhibited and NF-κB and STAT3 activities were significantly lowered in the CAIA and LPS-treated IL-32β transgenic mice. The expression of pro-inflammatory proteins was prevented in the paw tissues of CAIA and LPS-treated IL-32β transgenic mice. In addition, IL-32β altered several cytokine levels in the blood, spleen and paw joint. Our data indicates that IL-32β comprehensively inhibits the inflammation responses in the CAIA and LPS-induced inflammatory arthritis model.
    Oncotarget 10/2015; DOI:10.18632/oncotarget.6160 · 6.36 Impact Factor
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    ABSTRACT: A new oplopane-type sesquiterpenoid tussilagofarin (1) and a new chromone tussilagofarol (2), along with 18 known compounds 3-20, were isolated from the flower buds of Tussilago farfara. The structures of the new compounds were elucidated on the basis of 1D and 2D NMR and HRESIMS data. Of the isolated compounds, oplopane- and bisabolane-type sesquterpenoids 1, 8-12, 15, and 16 were found to inhibit nitric oxide production in LPS-induced RAW 264.7 cells with IC50 values of 3.5-28.5 μM.
    Archives of Pharmacal Research 10/2015; DOI:10.1007/s12272-015-0667-7 · 2.05 Impact Factor
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    ABSTRACT: In our previous study, we found that (E)-2,4-bis(p-hydroxyphenyl)-2-butenal showed anti-cancer effect, but it showed lack of stability and drug likeness. We have prepared several (E)-2,4-bis(p-hydroxyphenyl)-2-butenal analogues by Heck reaction. We selected two compounds which showed significant inhibitory effect of colon cancer cell growth. Thus, we evaluated the anti-cancer effects and possible mechanisms of one compound (E)-4-(3-(3,5-dimethoxyphenyl)allyl)-2-methoxyphenol in vitro and in vivo. In this study, we found that (E)-4-(3-(3,5-dimethoxyphenyl)allyl)-2-methoxyphenol induced apoptotic cell death in a dose dependent manner (0-15 μg/ml) through activation of Fas and death receptor (DR) 3 in HCT116 and SW480 colon cancer cell lines. Moreover, the combination treatment with (E)-4-(3-(3,5-dimethoxyphenyl)allyl)-2-methoxyphenol and nuclear factor κB (NF-κB) inhibitor, phenylarsine oxide (0.1 μM) or signal transducer and activator of transcription 3 (STAT3) inhibitor, Stattic (50 μM) increased the expression of Fas and DR3 more significantly. In addition, (E)-4-(3-(3,5-dimethoxyphenyl)allyl)-2-methoxyphenol suppressed the DNA binding activity of both STAT3 and NF-κB. Knock down of STAT3 or NF-κB p50 subunit by STAT3 small interfering RNA (siRNA) or p50 siRNA magnified (E)-4-(3-(3,5-dimethoxyphenyl)allyl)-2-methoxyphenol-induced inhibitory effect on colon cancer cell growth. Besides, the expression of Fas and DR3 was increased in STAT3 siRNA or p50 siRNA transfected cells. Moreover, docking model and pull-down assay showed that (E)-4-(3-(3,5-dimethoxyphenyl)allyl)-2-methoxyphenol directly bound to STAT3 and NF-κB p50 subunit. Furthermore, (E)-4-(3-(3,5-dimethoxyphenyl)allyl)-2-methoxyphenol inhibited colon tumor growth in a dose dependent manner (2.5 mg/kg-5 mg/kg) in mice. Therefore, these findings indicated that (E)-4-(3-(3,5-dimethoxyphenyl)allyl)-2-methoxyphenol may be a promising anti-cancer agent for colon cancer with more advanced research.
    Oncotarget 10/2015; DOI:10.18632/oncotarget.5861 · 6.36 Impact Factor
  • Haeun Kim · Jin Tae Hong · Mi Hee Park ·

    09/2015; 16(3):121-128. DOI:10.12729/jbr.2015.16.3.121
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    ABSTRACT: Alzheimer's disease (AD) and depression in late life are one of the most severe health problems in the world disorders. Serotonin 6 receptor (5-HT6R) has caused much interest for potential roles in AD and depression. However, a causative role of perturbed 5-HT6R function between two diseases was poorly defined. In the present study, we found that a 5-HT6R antagonist, SB271036 rescued memory impairment by attenuating the generation of Aß via the inhibition of ?-secretase activity and the inactivation of astrocytes and microglia in the AD mouse model. It was found that the reduction of serotonin level was significantly recovered by SB271036, which was mediated by an indirect regulation of serotonergic neurons via GABA. Selective serotonin reuptake inhibitor (SSRI), fluoxetine significantly improved cognitive impairment and behavioral changes. In human brain of depression patients, we then identified the potential genes, amyloid beta (A4) precursor protein-binding, family A, member 2 (APBA2), well known AD modulators by integrating datasets from neuropathology, microarray, and RNA seq. studies with correlation analysis tools. And also, it was demonstrated in mouse models and patients of AD. These data indicate functional network of 5-HT6R between AD and depression.
    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
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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
  • Hyung-Mun Yun · Kyung-Ran Park · Eun-Cheol Kim · Jin Tae Hong ·
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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

  • 06/2015; 48(3):301-307. DOI:10.5657/KFAS.2015.0301
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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

Publication Stats

5k Citations
1,011.49 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
  • 1998-2011
    • Korea Food and Drug Administration
      Seishō-gun, North Gyeongsang, South Korea
  • 2010
    • Konkuk University
      • Bio/Molecular Informatics Center
      Sŏul, Seoul, South Korea
  • 2008
    • Safety Research Institute
      Georgia, United States
  • 2006
    • Soonchunhyang University
      Onyang, Chungcheongnam-do, South Korea
  • 2003
    • Ewha Womans University
      Sŏul, Seoul, South Korea
  • 1993
    • Korea Institute of Toxicology
      Sŏul, Seoul, South Korea