中國醫藥大學機構典藏 China Medical University Repository, Taiwan:Item 310903500/30642
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    题名: Genetic analysis of two subspecies of reeves' Muntjac (Cervidae : Muntiacus reevesi) by Karyotyping and satellite DNA analyses
    作者: Chiang, PY;Lin, CC;Lia, SJ;Hsieh, LJ;Li, SY;Chao, MC;Li, YC
    贡献者: 附設醫院醫研部;Chung Shan Med Univ, Dept Life Sci, Taichung 402, Taiwan;China Med Univ Hosp, Dept Med Res, Taichung 404, Taiwan;Univ Alberta, Dept Med & Pathol, Edmonton, AB T6G 2B7, Canada;Taipei Zoo, Taipei 116, Taiwan
    日期: 2004
    上传时间: 2010-09-24 14:59:12 (UTC+8)
    出版者: ACAD SINICA INST ZOOLOGY
    摘要: Proliferation of vascular smooth muscle cells (VSMCs) is postulated to be one of the key events in the pathogenesis of atherosclerosis and restenosis. We investigated whether YD-3, a low-molecular weight, non-peptide compound, could modulate proliferation of VSMCs in vitro and restenosis after balloon angio-plasty in vivo. We examined the effect of YD-3 on thrombin-induced VSMC proliferation by [H-3]thymidine incorporation assay. The data demonstrated that YD-3 inhibited VSMC proliferation in a concentration-dependent manner. To define the mechanisms of YD-3 action, we found that YD-3 showed a profound inhibition on thrombin-induced Ras and ERK 1/2 activities by using Western blotting analysis. Furthermore, oral administration of YD-3 exhibited a marked reduction in neointimal thickness using the carotid injury model in rats. Using immuno-chemical detection, our experiments also revealed that YD-3 significantly suppressed expression of the PAR-I receptor, and markedly inhibited PAR-I-activating peptide (SFLLRN)-induced VSMC proliferation in a concentration-dependent manner. These results suggest that YD-3 inhibits thrombin-induced VSMC growth via the Ras- and ERK 1/2-mediated signaling pathway. Moreover, YD-3 also shows a developmental potential in the treatment of atherosclerosis and restenosis after vascular injury.
    關聯: ZOOLOGICAL STUDIES 43(4):749-758
    显示于类别:[台中附設醫院] 期刊論文

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