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    題名: 14-membered cyclopeptides from Paliurus ramosissimus and P-hemsleyanus
    作者: Lin, HY;Chen, CH;Liu, KCSC;Lee, SS
    貢獻者: 藥學院藥學系;Natl Taiwan Univ, Coll Med, Sch Pharm, Taipei 100, Taiwan;China Med Coll, Dept Pharm, Taichung, Taiwan
    日期: 2003
    上傳時間: 2010-09-24 18:55:58 (UTC+8)
    出版者: WILEY-V C H VERLAG GMBH
    摘要: 1 Magnolol, an active component isolated from the root and stein bark of Magnolia officinalis, has been reported to exhibit antitumour effects, but little is known about its molecular mechanisms of action. 2 Magnolol inhibited proliferation of human lung squamous carcinoma CH27 cells at low concentrations (10 - 40 muM), and induced apoptosis at high concentrations (80 - 100 muM). 3 Treatment with 80 muM magnolol significantly increased the expression of Bad and Bcl-X-S proteins, whereas it decreased the expression of Bcl-X-L. Overexpression of Bcl-2 protected CH27 cells against magnolol-triggered apoptosis. 4 Magnolol treatment resulted in accumulation of cytosolic cytochrome c and activation of caspase-9 and downstream caspases (caspase-3 and -6). Pretreatment with z-VAD-fmk markedly inhibited magnolol-induced cell death, but did not prevent cytosolic cytochrome c accumulation. 5 Magnolol induced a modest and persistent JNK activation and ERK inactivation in CH27 cells without evident changes in the protein levels. The responsiveness of JNK and ERK to magnolol suggests the involvement of these kinases in the initiation of the apoptosis process. 6 These results indicate that regulation of the Bcl-2 family, accumulation of cytosolic cytochrome c, and activation of caspase-9 and caspase-3 may be the effector mechanisms of magnolol-induced apoptosis.
    關聯: HELVETICA CHIMICA ACTA 86(1):127-138
    顯示於類別:[藥學系暨碩博士班] 期刊論文

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