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Yang, Woo Seok,Yang, Eunju,Kim, Min-Jeong,Jeong, Deok,Yoon, Deok Hyo,Sung, Gi-Ho,Lee, Seungihm,Yoo, Byong Chul,Yeo, Seung-Gu,Cho, Jae Youl World Scientific Publishing Company 2018 The American journal of Chinese medicine Vol.46 No.2
<P><I>Momordica charantia</I> known as bitter melon is a representative medicinal plant reported to exhibit numerous pharmacological activities such as antibacterial, antidiabetic, anti-inflammatory, anti-oxidant, antitumor, and hypoglycemic actions. Although this plant has high ethnopharmacological value for treating inflammatory diseases, the molecular mechanisms by which it inhibits the inflammatory response are not fully understood. In this study, we aim to identify the anti-inflammatory mechanism of this plant. To this end, we studied the effects of its methanol extract (Mc-ME) on lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages. Specifically, we evaluated nitric oxide (NO) production, mRNA expression of inflammatory genes, luciferase reporter gene activity, and putative molecular targets. Mc-ME blocked NO production in a dose-dependent manner in RAW264.7 cells; importantly, no cytotoxicity was observed. Moreover, the mRNA expression levels of inducible NO synthase (iNOS) and cyclooxygenase (COX)-2 were decreased by Mc-ME treatment in a dose-dependent manner. Luciferase assays and nuclear lysate immunoblotting analyses strongly indicated that Mc-ME decreases the levels of p65 [a nuclear factor (NF)-<TEX>$ \kappa $</TEX>B subunit] and c-Fos [an activator protein (AP)-1 subunit]. Whole lysate immunoblotting assays, luciferase assays, and overexpression experiments suggested that transforming growth factor <TEX>$ \beta $</TEX>-activated kinase 1 (TAK1) is targeted by Mc-ME, thereby suppressing NF-<TEX>$ \kappa $</TEX>B and AP-1 activity via downregulation of extracellular signal-regulated kinases (ERKs) and AKT. These results strongly suggest that Mc-ME exerts its anti-inflammatory activity by reducing the action of TAK1, which also affects the activation of NF-<TEX>$ \kappa $</TEX>B and AP-1.</P>
Yang, Sungjae,Kim, Yong,Jeong, Deok,Kim, Jun Ho,Kim, Sunggyu,Son, Young-Jin,Yoo, Byong Chul,Jeong, Eun Jeong,Kim, Tae Woong,Han Lee, In-Sook,Cho, Jae Youl The Korean Society of Applied Pharmacology 2016 Biomolecules & Therapeutics(구 응용약물학회지) Vol.24 No.6
(E)-3-Phenyl-1-(2-pyrrolyl)-2-propenone (PPP) is a pyrrole derivative of chalcone, in which the B-ring of chalcone linked to ${\beta}$-carbon is replaced by pyrrole group. While pyrrole has been studied for possible Src inhibition activity, chalcone, especially the substituents on the B-ring, has shown pharmaceutical, anti-inflammatory, and anti-oxidant properties via inhibition of NF-${\kappa}B$ activity. Our study is aimed to investigate whether this novel synthetic compound retains or enhances the pharmaceutically beneficial activities from the both structures. For this purpose, inflammatory responses of lipopolysaccharide (LPS)-treated RAW264.7 cells were analyzed. Nitric oxide (NO) production, inducible NO synthase (iNOS) and tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$) mRNA expression, and the intracellular inflammatory signaling cascade were measured. Interestingly, PPP strongly inhibited NO release in a dose-dependent manner. To further investigate this anti-inflammatory activity, we identified molecular pathways by immunoblot analyses of nuclear fractions and whole cell lysates prepared from LPS-stimulated RAW264.7 cells with or without PPP pretreatment. The nuclear levels of p50, c-Jun, and c-Fos were significantly inhibited when cells were exposed to PPP. Moreover, according to the luciferase reporter gene assay after cotransfection with either TRIF or MyD88 in HEK293 cells, NF-${\kappa}B$-mediated luciferase activity dose-dependently diminished. Additionally, it was confirmed that PPP dampens the upstream signaling cascade of NF-${\kappa}B$ and AP-1 activation. Thus, PPP inhibited Syk, Src, and TAK1 activities induced by LPS or induced by overexpression of these genes. Therefore, our results suggest that PPP displays anti-inflammatory activity via inhibition of Syk, Src, and TAK1 activity, which may be developed as a novel anti-inflammatory drug.
Middle East Respiratory Syndrome in 3 Persons, South Korea, 2015
Yang, Jeong-Sun,Park, SungHan,Kim, You-Jin,Kang, Hae Ji,Kim, Hak,Han, Young Woo,Lee, Han Saem,Kim, Dae-Won,Kim, A-Reum,Heo, Deok Rim,Kim, Joo Ae,Kim, Su Jin,Nam, Jeong-Gu,Jung, Hee-Dong,Cheong, Hyang- U.S. Department of Health and Human Services * Cen 2015 Emerging Infectious Diseases Vol.21 No.11
<P>In May 2015, Middle East respiratory syndrome coronavirus infection was laboratory confirmed in South Korea. Patients were a man who had visited the Middle East, his wife, and a man who shared a hospital room with the index patient. Rapid laboratory confirmation will facilitate subsequent prevention and control for imported cases.</P>
( Sungjae Yang ),( Yong Kim ),( Deok Jeong ),( Jun Ho Kim ),( Sunggyu Kim ),( Young-jin Son ),( Byong Chul Yoo ),( Eun Jeong Jeong ),( Tae Woong Kim ),( In-sook Han Lee ),( Jae Youl Cho ) 한국응용약물학회 2016 Biomolecules & Therapeutics(구 응용약물학회지) Vol.24 No.6
(E)-3-Phenyl-1-(2-pyrrolyl)-2-propenone (PPP) is a pyrrole derivative of chalcone, in which the B-ring of chalcone linked to bcarbon is replaced by pyrrole group. While pyrrole has been studied for possible Src inhibition activity, chalcone, especially the substituents on the B-ring, has shown pharmaceutical, anti-inflammatory, and anti-oxidant properties via inhibition of NF-kB activity. Our study is aimed to investigate whether this novel synthetic compound retains or enhances the pharmaceutically beneficial activities from the both structures. For this purpose, inflammatory responses of lipopolysaccharide (LPS)-treated RAW264.7 cells were analyzed. Nitric oxide (NO) production, inducible NO synthase (iNOS) and tumor necrosis factor-a (TNF-a) mRNA expression, and the intracellular inflammatory signaling cascade were measured. Interestingly, PPP strongly inhibited NO release in a dose-dependent manner. To further investigate this anti-inflammatory activity, we identified molecular pathways by immunoblot analyses of nuclear fractions and whole cell lysates prepared from LPS-stimulated RAW264.7 cells with or without PPP pretreatment. The nuclear levels of p50, c-Jun, and c-Fos were significantly inhibited when cells were exposed to PPP. Moreover, according to the luciferase reporter gene assay after cotransfection with either TRIF or MyD88 in HEK293 cells, NF-kB-mediated luciferase activity dose-dependently diminished. Additionally, it was confirmed that PPP dampens the upstream signaling cascade of NF-kB and AP-1 activation. Thus, PPP inhibited Syk, Src, and TAK1 activities induced by LPS or induced by overexpression of these genes. Therefore, our results suggest that PPP displays anti-inflammatory activity via inhibition of Syk, Src, and TAK1 activity, which may be developed as a novel anti-inflammatory drug.
Analysis of SOHOS Flash Memory with 3-level Charge Pumping Method
Yang, Seung-Dong,Kim, Seong-Hyeon,Yun, Ho-Jin,Jeong, Kwang-Seok,Kim, Yu-Mi,Kim, Jin-Seop,Ko, Young-Uk,An, Jin-Un,Lee, Hi-Deok,Lee, Ga-Won The Institute of Electronics and Information Engin 2014 Journal of semiconductor technology and science Vol.14 No.1
This paper discusses the 3-level charge pumping (CP) method in planar-type Silicon-Oxide-High-k-Oxide-Silicon (SOHOS) and Silicon-Oxide-Nitride-Oxide-Silicon (SONOS) devices to find out the reason of the degradation of data retention properties. In the CP technique, pulses are applied to the gate of the MOSFET which alternately fill the traps with electrons and holes, thereby causing a recombination current Icp to flow in the substrate. The 3-level charge pumping method may be used to determine not only interface trap densities but also capture cross sections as a function of trap energy. By applying this method, SOHOS device found to have a higher interface trap density than SONOS device. Therefore, degradation of data retention characteristics is attributed to the many interface trap sites.
Jeong, Seong-Gu,Kim, Sunggyu,Kim, Han Gyung,Kim, Eunji,Jeong, Deok,Kim, Ji Hye,Yang, Woo Seok,Oh, Junsang,Sung, Gi-Ho,Hossain, Mohammad Amjad,Lee, Jongsung,Kim, Jong-Hoon,Cho, Jae Youl Elsevier 2019 Journal of Ethnopharmacology Vol.231 No.-
<P><B>Abstract</B></P> <P><B>Ethnopharmacological relevance</B></P> <P> <I>Mycetia cauliflora</I> Reinw. (Rubiaceae) has been used as a traditional remedy to ameliorate clinical signs of inflammatory diseases, including pain, inflammation, ulcers, and wounds. Among the Mycetia subfamilies, the molecular and cellular mechanisms of <I>Mycetia longifolia</I> (Rubiaceae) have been studied. However, those of <I>Mycetia cauliflora</I> are not clearly understood. Comprehensive investigation of this plant is necessary to evaluate its potential for ethnopharmacological use.</P> <P><B>Materials</B></P> <P>and methods: The activities of <I>Mycetia cauliflora</I> methanol extract (Mc-ME) on the secretion of inflammatory mediators, the mRNA expression of proinflammatory cytokines, and identification of its molecular targets were elucidated using lipopolysaccharide (LPS)-induced macrophage-like cells. Moreover, the suppressive actions of Mc-ME were examined in an LPS-induced peritonitis mouse model.</P> <P><B>Results</B></P> <P>At nontoxic concentrations, Mc-ME downregulated the release of nitric oxide (NO), the mRNA expression of inducible nitric oxide synthase (iNOS), and the mRNA expression of interleukin (IL)-1β from LPS-activated RAW264.7 cells. This extract also inhibited the nuclear translocation of p65 and p50 and the phosphorylation of IκBα, IKK, and AKT. Western blot analysis and <I>in vitro</I> kinase assays confirmed that phosphoinositide-dependent kinase-1 (PDK1) is the direct immunopharmacological target of Mc-ME effect. In addition, Mc-ME significantly reduced inflammatory signs in an animal model of acute peritonitis. These effects were associated with decreased NO production and decreased AKT phosphorylation.</P> <P><B>Conclusion</B></P> <P>Our results suggest that Mc-ME displays anti-inflammatory actions in LPS-treated macrophage-like cells and in an animal model of acute inflammatory disease. These actions are preferentially managed by targeting PDK1 in the nuclear factor (NF)-κB signaling pathway.</P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>