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收集所有交通大學研究人員與學生個人或團體所發表之各項學術著作，涵蓋期刊論文、教師專書、學位論文等項。;;Collections of Publications of NCTU Researchers and Students Like Journal Papers and Thesis.

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🏛️國立陽明交通大學機構典藏

Author: search.filters.author.Wu, CHSubject: search.filters.subject.restenosis

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    The molecular mechanism of actinomycin D in preventing neointimal formation in rat carotid arteries after balloon injury
    (2005-05-01)
    Wu, CH
    ;
    Pan, JS
    ;
    Chang, WC
    ;
    Hung, JS
    ;
    Mao, SJT
    The pathological mechanism of restenosis is primarily attributed to excessive proliferation of vascular smooth muscle cells (SMC). Actinomycin D has been regarded as a potential candidate to prevent balloon injury-induced neointimal formation. To explore its molecular mechanism in regulating cell proliferation, we first showed that actinomycin D markedly reduced the SMC proliferation via the inhibition of BrdU incorporation at 80 nM. This was further supported by the G1-phase arrest using a flowcytometric analysis. Actinomycin D was extremely potent with an inhibitory concentration IC50 at 0.4 nM, whereas the lethal dose LD50 was at 260 mu M. In an in vivo study, the pluronic gel containing 80 nM and 80 lMactinomycin D was applied topically to surround the rat carotid adventitia; the thickness of neointima was substantially reduced (45 and 55%, respectively). The protein expression levels of proliferating cell nuclear antigen ( PCNA), focal adhesion kinase (FAK), and Raf were all suppressed by actinomycin D. Extracellular signal-regulated kinases (Erk) involved in cell-cycle arrest were found to increase by actinomycin D. These observations provide a detailed mechanism of actinomycin D in preventing cell proliferation thus as a potential intervention for restenosis.
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    The preventive effects of G115 on balloon injury-induced neointima formation in rats
    (2001-12-28)
    Wu, CH
    ;
    Tsai, BR
    ;
    Hsieh, WT
    ;
    Chang, GY
    ;
    Mao, SJT
    After percutaneous transluminal coronary angioplasty (PTCA), 30-50% of the patients may present with restenosis within 6 months. The aim of this study was to search for a preventive remedy against the balloon injury-induced neointima formation. Ginseng, with its wide indications on immune and cardiovascular functions, has prompted us to explore its role in neointima formation. In the present study, we aimed to explore if a standardized Panax Ginseng extract G115 was able to inhibit neointimal formation. With BrdU luminencence assay, maximal proliferation of rat smooth muscle cells was reduced to 24% of control values by G115. Norepinephrine-induced vasocontraction was antagonized in 21% and 44% by 1.44mg/ml and 2.88mg/ml of G115, respectively. Neointima-to-lumen area ratio of balloon-injured rat carotid arteries was reduced 77.3% by G115 as compared to the sham control. These results demonstrate the preventive effects of ginsenosides on angioplasty-mediated neointima formation. (C) 2001 Elsevier Science Inc. All rights reserved.