• Tuberculosis and Respiratory Diseases
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• v.61 no.4
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• pp.366-373
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• 2006

Background: Paraquat is extremely toxic chemical material, which generates reactive oxygen species (ROS), causing multiple organ failure. In particular, paraquat leads to irreversible progressive pulmonary fibrosis. Exaggerated cell deaths exceeding the normal repair of type II pneumocytes leads to mesenchymal cells proliferation and fibrosis. This study examined the followings; i) whether or not paraquat induces cell death in lung epithelial cells; ii) whether or not paraquat-induced cell deaths are apoptosis or necrosis; and iii) the effects of N-acetylcysteine, dexamethasone, and bcl-2 on paraquat-induced cell deaths. Methods: A549 and BEAS-2B lung epithelial cell lines were used. The cell viability and apoptosis were evalluated using a MTT assay, Annexin V staining was monitored by fluorescence microscopy, The level of bcl-2 inhibition was examined by establishing stable A549 pcDNA3-bcl-2 cell lines throung the transfection of pcDNA3-bcl-2 with the mock. Results: Paraquat decreased the cell viability in A549 and BEAS-2B cells in a dose and time dependent manner. The Annexin V assay showed that apoptosis was the type of paraquat-induced cell death. Paraquat-induced cell deaths was significantly inhibited by N-acetylcysteine, dexamethasone, and bcl-2 overexpression. The cell viability of A549 cells treated with N-acetylcysteine, and dexamethasone on the paraquat-induced cell deaths were increased significantly by 10 ~ 20%, particularly at high doses. In addition, the cell viability of A549 pcDNA3-bcl-2 cells overexpressing bcl-2 was significantly higher than the untransfected A549 cells. Conclusion: Paraquat induces apoptotic cell deaths in lung epithelial cells in a dose and time dependent manner. The paraquat-induced apoptosis of lung epithelial cells might occur through the mitochondrial pathway.

• Journal of Apiculture
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• v.34 no.3
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• pp.245-254
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• 2019

We investigated the anti-tumor effects and molecular mechanism of Brazil, China and Korean regional propolis on HeLa ovarian cancer cell line. Each propolis extracts was prepared by ethanol extraction method. Cytotoxicity of propolis extracts was determinated by EZ-cytox cell viability assay. To necessity of anti-tumor effect and molecular mechanism of propolis, we must be adjusting propolis concentration. Due to 100 ㎍/mL of propolis extract were reduced cell viability to less than 50%, we adjusted all of propolis concentration to 100 ㎍/mL. By Western blotting analysis, we confirmed that anti-tumor mechanism of Brazil, China and Korea regional propolis has significantly difference. All of propolis was activated apoptosis related molecules such as PARP, caspase-3. However, cell proliferation signaling molecules including Akt1, ERK and Bcl-2 were reduced the protein expression level. Especially, the expression of tumor suppressor protein p53 was significantly increased in propolis-treated group such as Gyeonggi, Chungbuk, Chungnam, Jeonbuk, Gyeongnam and China. The phosphorylation of Bax which as apoptosis indicator was appeared in propolis-treated group such as Gyeonggi, Gangwon, Chungnam, Gyeongbuk, China. In this results showed that the regional propolis has completely different mechanism in anti-tumor. Thus, propolis extracts may be useful source of functional materials on anti-cancer and it will be able to choose the suitable propolis for cancer therapy by analyzing individual characteristics.

• Journal of the Society of Cosmetic Scientists of Korea
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• v.41 no.4
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• pp.375-382
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• 2015

Ginsenosides (ginseng saponin) as the one of important pharmaceutical compounds of ginseng and is responsible for the pharmacological and biological activities. These ginsenoside produces diverse small molecules ginsenoside which have more pharmacological activities including anti-wrinkle, anti-cancer and anti-oxidant effects. In the present study, we isolated bacteria using esculin agar, to produce ${\beta}$-glucosidase, and we focused on the bio-transformation of ginsenoside. Phylogenetic tree analysis was performed by comparing the 16S rRNA sequences; we identified the strain as Stenotrophomonas rhizopilae strain GFC09. In order to determine the optimal conditions for enzyme activity, the crude enzyme was incubated with 1 mM ginsenoside $Rb_1$. Bioconversion of ginsenoside $Rb_1$ were analyzed using TLC and HPLC. The crude enzyme hydrolyzed the ginsenoside $Rb_1$ along the following pathway: LB: $Rb_1{\rightarrow}Rd{\rightarrow}F_2$ into compound K, TSB: $Rb_1{\rightarrow}Rd{\rightarrow}F_2$. The structure of the hydrolyzed metabolites were identified by NMR. The activity screening tests showed that the conversion product induced the production of type I procollagen in a dose-dependent manner. These results suggested that hydrolyzed ginseng product containing the ginsenoside $F_2$ and compound K could be useful as an active ingredient for wrinkle-care cosmetics.

• Journal of Life Science
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• v.28 no.11
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• pp.1268-1276
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• 2018

The cytidine analog decitabine (DEC) acts as a nucleic acid synthesis inhibitor, whereas ammonium pyrrolidine dithiocarbamate (PDTC) is an inhibitor of nuclear factor-${\kappa}B$. The aim of this study was to investigate the possible synergistic inhibitory effect of these two inhibitors on proliferation of human gastric cancer AGS cells. The inhibitory effect of PDTC on AGS cell proliferation was significantly increased by DEC in a concentration-dependent manner, and this inhibition was associated with cell cycle arrest at the G2/M phase and the induction of apoptosis. This induction of apoptosis by the co-treatment with PDTC and DEC was related to the induction of DNA damage, as assessed by H2AX phosphorylation. Further studies demonstrated that co-treatment with PDTC and DEC induced the disruption of mitochondrial membrane potential, increased the generation of intracellular reactive oxygen species (ROS) and the expression of pro-apoptotic Bax, and down-regulated the expression of anti-apoptotic Bcl-2, ultimately resulting in the release of cytochrome c from the mitochondria into the cytoplasm. Co-treatment with PDTC and DEC also activated caspase-8 and caspase-9, which are representative caspases of the extrinsic and intrinsic apoptosis pathways. Co-treatment also activated caspase-3, which was accompanied by proteolytic degradation of poly (ADP-ribose) polymerase. Taken together, these data clearly indicated that co-treatment with PDTC and DEC suppressed the proliferation of AGS cells by increasing DNA damage and activating the ROS-mediated extrinsic and intrinsic apoptosis pathways.

• Journal of Life Science
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• v.33 no.5
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• pp.397-405
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• 2023

Although glutathione (GSH) has been shown to play an important role in the prevention of oxidative damage as an antioxidant, studies on immune regulation by it have not been properly conducted. In this study, we investigated whether luthione^®, a reduced GSH, has an immune enhancing effect in murine macrophage RAW 264.7 cells. The results of flow cytometry and immunofluorescence experiments indicated that luthione increased phagocytic activity, a representative function of macrophages, compared to the control cells. According to the results of the cytokine array, the expression of interleukin (IL)-5, IL-1β, and IL-27 was significantly increased in the luthione-treated cells. Luthione also enhanced the production of tumor necrosis factor-α and IL-1β through increased expression of their proteins, and increased release of the immune mediators such as nitric oxide (NO) and prostaglandin E₂ was associated with increased expression of inducible NO synthase and cyclooxygenase-2. In addition, the expression of cluster of differentiation 86, an M1 macrophage marker, was dramatically enhanced in RAW 264.7 cells treated with luthione. Furthermore, as a result of heat map analysis, we found that cytokine signaling 1/3-mediated signal transducer and activator of transcription/Janus tyrosine kinase signaling pathway was involved in the immunomodulatory effect by luthione. In conclusion, our data suggested that luthione could act as a molecular regulator in M1 macrophage polarization and enhance immune capacity by promoting macrophage phagocytic function.

• Korean Journal of Plant Resources
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• v.35 no.5
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• pp.565-573
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• 2022

Gingival inflammation is one of the main causes that can be related to various periodontal diseases. Human gingival fibroblast (HGF) is the major constituent in periodontal connective tissue and secretes various inflammatory mediators, such as nitric oxide (NO) and prostaglandin E₂ (PGE₂), upon lipopolysaccharide stimulation. This study is aimed at investigating the anti-inflammatory and antioxidative activities of Lotus Root extract (LRE) in Porphyromonas gingivalis derived lipopolysaccharide (LPS-PG)-stimulated HGF-1 cells. The concentration of NO and PGE₂, as well as their responsible enzymes, inducible NO synthase (iNOS), and cyclooxygenase-2 (COX-2), was analyzed by Griess reaction, ELISA, and western blot analysis. LPS-PG sharply elevated the production and protein expression of inflammatory mediators, which were significantly attenuated by LRE treatment in a dose-dependent manner. LRE treatment also suppressed activation of Toll-like receptor 4 (TLR4)/myeloid differentiation primary response gene 88 (MyD88) and nuclear factor-κB (NF-κB) in LPS-PG-stimulated HGF-1 cells. In addition, one of phase II enzyme, NAD(P)H quinone dehydrogenase (NQO)-1, and its transcription factor, Nuclear factor erythroid 2-related factor 2 (Nrf2), were significantly induced by LRE treatment. Consequently, these results suggest that LRE ameliorates LPS-PG-induced inflammatory responses by attenuating TLR4/MyD88-mediated NF-κB, and activating NQO-1/Nrf2 antioxidant response element signaling pathways in HGF-1 cells.

• KSCE Journal of Civil and Environmental Engineering Research
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• v.35 no.3
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• pp.567-577
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• 2015

Climate and land use changes have impact on availability water resource by hydrologic cycle change. The purpose of this study is to evaluate the hydrologic behavior by the future potential climate and land use changes in Anseongcheon watershed ($371.1km^2$) using SWAT model. For climate change scenario, the HadGEM-RA (the Hadley Centre Global Environment Model version 3-Regional Atmosphere model) RCP (Representative Concentration Pathway) 4.5 and 8.5 emission scenarios from Korea Meteorological Administration (KMA) were used. The mean temperature increased up to $4.2^{\circ}C$ and the precipitation showed maximum 21.2% increase for 2080s RCP 8.5 scenario comparing with the baseline (1990-2010). For the land use change scenario, the Conservation of Land Use its Effects at Small regional extent (CLUE-s) model was applied for 3 scenarios (logarithmic, linear, exponential) according to urban growth. The 2100 urban area of the watershed was predicted by 9.4%, 20.7%, and 35% respectively for each scenario. As the climate change impact, the evapotranspiration (ET) and streamflow (ST) showed maximum change of 20.6% in 2080s RCP 8.5 and 25.7% in 2080s RCP 4.5 respectively. As the land use change impact, the ET and ST showed maximum change of 3.7% in 2080s logarithmic and 2.9% in 2080s linear urban growth respectively. By the both climate and land use change impacts, the ET and ST changed 19.2% in 2040s RCP 8.5 and exponential scenarios and 36.1% in 2080s RCP 4.5 and linear scenarios respectively. The results of the research are expected to understand the changing water resources of watershed quantitatively by hydrological environment condition change in the future.

• Journal of Food Hygiene and Safety
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• v.19 no.4
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• pp.176-184
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• 2004

This study was conducted to compare and estimate the daily PAHs dietary intake from both home-cooking and dining-out, through approach of model diet used in exposure assessment of food contaminants. Food commodities reflecting in model diet were selected from the KHIDI report and were analysed in cooked or uncooked edible forms using HPLC-Fluorscence Detector. The PAHs dietary intake comparison between home-cooking and dining-out was based on one meal intake suggested in model diet and PAHs dietary intake was estimated by using food consumption rate and body weight of the Korean adult group. The daily PAHs dietary intake was calculated by permutation and combination method with assumption that a person consumed 2 meals from home-cooking menu and 1 meal from dining-out menu. The total PAHs levels in 36 food commodities with 200 samples were ranged from 2.00 ug/kg to 141.28 ug/kg and a food showing the highest PAHs level was the stir-fried anchovy. The $TEQ_{BaP}$ levels of PAHs were calculated using benzo(a)pyrene equivalents individual congener level and corresponding TEF value and the $TEQ_{BaP}$ level were ranged from $0.03\;ugTEQ{BaP}$ to $1.31\;ugTEQ_{BaP}$ and a food showing the highest $TEQ_{BaP}$ level was the hamburger. The PAHs dietary intakes per one meal from home-cooking and dining-out were $2.4\times10^{-3}\;ugTEQ_{BaP}/kg/meal\;and\;4.0\times10^{-3}\;ugTEQ_{BaP}/kg/meal$, respectively. This data showed the PAHs dietary intake from dining-out was about 1.7 times higher than from the home-cooking. The daily PAHs dietary intakes of general Korean adult having two meals from home-cooking and one meal from dining-out per a day were ranged between $8.0\times10^{-3}\~9.7\times10^{-3}\;ugTEQ_{BaP}/gg/day$ and mean value as $8.9\times10^{-3}\~9.7\times10^{-3}\;ugTEQ_{BaP}/gg/day$.

• The Journal of the Petrological Society of Korea
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• v.12 no.1
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• pp.16-31
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• 2003

The granites in the southern Gimcheon area can be divided into two parts, marginal hornblende biotite granodiorite (Mgd) and central biotite granodiorite to granite (Cgd). Mgd and Cgd are gray in color and display gradational contact relations and are mainly composed of coarse-grained and medium-grained rocks, respectively. Mgd has more frequent and larger mafic enclaves than Cgd, and the two granites partly show parallel foliation at thire contact with gneisses. From representative samples of the granites, K-Ar biotite ages of 197∼207 Ma were obtained. Considering the blocking temperature of biotite, it is suggested that the emplacement age of the granitic magma was probably late Triassic. The anorthite contents of plagioclases in Mgd display less variation than those of Cgd, indicating that Mgd crystallized within a narrow range of temperatures. In the Al$\_$total/-Mg diagram, the biotites from the granites plot within the subalkaline field, and the smooth slope indicates differentiation from a single magma. All amphiboles from the granites belong to magnesio-hornblende. The linear trends of major oxides, AFM and Ba-Sr-Rb indicate that Mgd and Cgd were fractionally differentiated from a single granitic magma body crystallizing from the margin inwards. The relations of modal (Qz+Af) vs. Op, K$_2$O vs. Na$_2$O, Fe$_2$ $O_3$ vs. FeO, Fe$\^$+3/(Fe$\^$+3/+Fe$\^$+2/) and K/Rb vs. Rb/Sr show that they belong to I-type and magnetite-series granitic rocks developed by the progressive melting products of fixed sources. REE data, normalized to chondrite value, have trends of enriched LREE and depleted HREE together with weakly negative Eu anomalies.

• Tuberculosis and Respiratory Diseases
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• v.62 no.1
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• pp.33-42
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• 2007

Background: Heme oxygenase-1 (HO-1) is known to modulates the cellular functions, including cell proliferation and apoptosis. It is known that a high level of HO-1 expression is found in many tumors, and HO-1 plays an important role in rapid tumor growth on account of its antioxidant and antiapoptotic effects. Cisplatin is a widely used anti-cancer agent for the treatment of lung cancer. However, the development of resistance to cisplatin is a major obstacle to its use in clinical treatment. We previously demonstrated that inhibiting HO-1 expression through the transcriptional activation of Nrf2 induces apoptosis in A549 cells. The aim of this study was to determine of the inhibiting HO-1 enhance the chemosensitivity of A549 cells to cisplatin. Materials and Methods: The human lung cancer cell line, A549, was treated cisplatin, and the cell viability was measured by a MTT assay. The change in HO-1, Nrf2, and MAPK expression after the cisplatin treatment was examined by Western blotting. HO-1 inhibition was suppressed by ZnPP, which is a specific pharmacologic inhibitor of HO activity, and small interfering RNA (siRNA). Flow cytometry analysis and Western blot were performed in to determine the level of apoptosis. The level of hydrogen peroxide ($H_2O_2$) generation was monitored fluoimetrically using 2',7'-dichlorofluorescein diacetate. Results: The A549 cells showed more resistance to the cisplatin treatment than the other cell lines examined, whereas cisplatin increased the expression of HO-1 and Nrf2, as well as the phosphorylation of MAPK in a time-dependent fashion. Inhibitors of the MAPK pathway blocked the induction of HO-1 and Nrf2 by the cisplatin treatment in A549 cells. In addition, the cisplatin-treated A549 cells transfected with dither the HO-1 small interfering RNA (siRNA) or ZnPP, specific HO-1 inhibitor, showed in a more significantly decrease in viability than the cisplatin-only-treated group. The combination treatment of ZnPP and cisplatin caused in a marked increase in the ROS generation and a decrease in the HO-1 expression. Conclusion: Cisplatin increases the expression of HO-1, probably through the MAPK-Nrf2 pathway, and the inhibition of HO-1 enhances the chemosensitivity of A549 cells to cisplatin.