Jun-Young Lee

Chungbuk National University, Chinsen, North Chungcheong, South Korea

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Publications (3)6.74 Total impact

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    ABSTRACT: Nuclear factor (NF)-kappaB regulates a central common signaling for immunity and cell survival. Artemisolide (ATM) was previously isolated as a NF-kappaB inhibitor from a plant of Artemisia asiatica. However, molecular basis of ATM on NF-kappaB activation remains to be defined. Here, we demonstrate that ATM is a typical inhibitor of IkappaB kinase beta (IKKbeta), resulting in inhibition of lipopolysaccharide (LPS)-induced NF-kappaB activation in RAW 264.7 macrophages. ATM inhibited the kinase activity of highly purified IKKbeta and also LPS-induced IKK activity in the cells. Moreover, the effect of ATM on IKKbeta activity was completely abolished by substitution of Cys-179 residue of IKKbeta to Ala residue, indicating direct targeting site of ATM. ATM could inhibit IkappaBalpha phosphorylation in LPS-activated RAW 264.7 cells and subsequently prevent NF-kappaB activation. Further, we demonstrate that ATM down-regulates NF-kappaB-dependent TNF-alpha expression. Taken together, this study provides a pharmacological potential of ATM in NF-kappaB-dependent inflammatory disorders.
    Biochemical and Biophysical Research Communications 10/2007; 361(3):593-8. DOI:10.1016/j.bbrc.2007.07.069 · 2.28 Impact Factor
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    ABSTRACT: Aerial parts of Artemisia asiatica (Compositae) have been traditionally used as an oriental medicine for the treatment of inflammatory and ulcerogenic diseases. In the present study, artemisolide was isolated as a nuclear factor (NF)-kappaB inhibitor from A. asiatica by activity-guided fractionation. Artemisolide inhibited NF-kappaB transcriptional activity in lipopolysaccharide (LPS)-stimulated macrophages RAW 264.7 with an IC50 value of 5.8 microM. The compound was also effective in blocking NF-kappaB transcriptional activities elicited by the expression vector encoding the NF-kappaB p65 or p50 subunits bypassing the inhibitory kB degradation signaling NF-kappaB activation. The macrophages markedly increased their PGE2 and NO production upon exposure to LPS alone. Artemisolide inhibited LPS-induced PGE2 and NO production with IC50 values of 8.7 microM and 6.4 microM, respectively, but also suppressed LPS-induced synthesis of cyclooxygenase (COX)-2 or inducible NO synthase (iNOS). Taken together, artemisolide is a NF-kappaB inhibitor that attenuates LPS-induced production of PGE2 or NO via down-regulation of COX-2 or iNOS expression in macrophages RAW 264.7. Therefore, artemisolide could represent and provide the anti-inflammatory principle associated with the traditional medicine, A. asiatica.
    Archives of Pharmacal Research 08/2006; 29(7):591-7. DOI:10.1007/BF02969271 · 1.75 Impact Factor
  • Hyun-Mo Shin · Yong Rok Lee · Yoon Sook Chang · Jun-Young Lee · Byung Hak Kim · Kyung Rak Min · Youngsoo Kim
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    ABSTRACT: Furonaphthoquinone compounds have been reported to exhibit anticancer, antibacterial and antiviral properties. The molecular basis for these diverse properties is not known. 2-Methyl-2-(2-methylpropenyl)-2,3-dihydronaphthoquinone [2,3-b]furan-4,9-dione (NFD-37) is a synthetic furonaphthoquinone compound. In the present study, NFD-37 was found to inhibit interleukin (IL)-6 production in lipopolysaccharide (LPS)-stimulated murine macrophages RAW 264.7. Further, NFD-37 attenuated LPS-induced synthesis of IL-6 transcript but also inhibited LPS-induced IL-6 promoter activity. Since nuclear factor (NF)-κB activation has been shown to play a key role in LPS-induced IL-6 expression, the effect of NFD-37 on LPS-induced NF-κB activation was further analyzed. NFD-37 exhibited a dose-dependent inhibitory effect on LPS-induced phosphorylation of inhibitory κBα protein (IκBα), and subsequently inhibited LPS-induced IκBα degradation as well as NF-κB transcriptional activity. In another experiment, NFD-37 inhibited both IL-6 promoter activity and NF-κB transcriptional activity elicited by an expression vector encoding IκB kinase β. Taken together, NFD-37 down-regulated LPS-induced IL-6 expression through NF-κB activation, which could provide a pharmacological basis for the anti-inflammatory properties of furonaphthoquinone analogs.
    International Immunopharmacology 07/2006; 6(6-6):916-923. DOI:10.1016/j.intimp.2006.01.006 · 2.71 Impact Factor