Yonsei Fraunhofer IZFP Medical Device Lab YFMED

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  • Publication
    Coptis japonica Makino extract suppresses Angiogenesis through regulation of cell cycle-related proteins
    ( 2016)
    Kim, S.H.
    ;
    Kim, E.-C.
    ;
    Kim, W.-J.
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    Lee, M.-H.
    ;
    Kim, S.-Y.
    ;
    Kim, T.-J.
    Angiogenesis, neovascularization from pre-existing vessels, is a key step in tumor growth and metastasis, and anti-angiogenic agents that can interfere with these essential steps of cancer development are a promising strategy for human cancer treatment. In this study, we characterized the anti-angiogenic effects of Coptis japonica Makino extract (CJME) and its mechanism of action. CJME significantly inhibited the proliferation, migration, and invasion of vascular endothelial growth factor (VEGF)-stimulated HUVECs. Furthermore, CJME suppressed VEGF-induced tube formation in vitro and VEGF-induced microvessel sprouting ex vivo. According to our study, CJME blocked VEGF-induced cell cycle transition in G1. CJME decreased expression of cell cycle-regulated proteins, including Cyclin D, Cyclin E, Cdk2, and Cdk4 in response to VEGF.
  • Publication
    Effect of nodakenin on atopic dermatitis-like skin lesions
    ( 2014)
    Park, S.-J.
    ;
    Cha, H.-S.
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    Lee, Y.-H.
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    Kim, W.-J.
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    Kim, D.-H.
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    Kim, E.-C.
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    Lee, K.-H.
    ;
    Kim, T.-J.
    Nodakenin, derived from the roots of Angelica gigas Nakai, is an important natural resource and medicinal material with anti-allergic and anti-inflammatory activities. We have previously shown that nodakenin inhibits IgE/Ag-induced degranulation in mast cells. In this study, we investigated the inhibitory effect of nodakenin on 2,4-dinitrochloro-benzene (DNCB)-induced atopic dermatitis (AD)-like skin lesions in ICR mice. Scratching behavior, skin severity score, blood IgE level, and skin thickness were improved in DNCB-induced AD-like ICR mice. Our results showed that nodakenin suppressed the increase of AD-like skin lesions in ICR mice. These results suggest that nodakenin may be a potential therapeutic resource for AD as well as an adjunctive agent to control itching associated with AD.