Chia Nan University of Pharmacy & Science Institutional Repository:Item 310902800/25161
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    標題: Possible Mechanism of Betel-quid-extract-induced Expression of Matrix Metalloproteinase-2
    作者: Yu-Chi Liu
    Mei-Huei Lin
    Shyun-Yeu Liu
    Wei-Fan Chiang
    Li-Lin Chen
    Tai-Chi Chen
    Yon-Chi Cheng
    Kai-Chen Hsu
    Pse-Chou Cheng
    Chin-Hai Lee
    Young-Chau Liu
    貢獻者: 生物科技系
    關鍵字: betel quid
    matrix metalloproteinase-2
    日期: 2010-11
    上傳時間: 2012-03-30 15:17:52 (UTC+8)
    摘要: Background/Purpose: Betel quid extract (BQE) has been demonstrated to induce matrix metalloproteinase
    (MMP)-2 expression. This study aimed to establish the possible mechanism involved in this event.
    Methods: Western blotting, reverse-transcription polymerase chain reaction, and gelatin zymography were
    used to study the expression level of MMP-2. LY294002, PD98059, U0126, N-acetyl-L-cysteine, SB203580,
    SP600125, and Bay 11-7082 were used to pretreat OECM-1 cells before BQE treatment and MMP-2 detection.
    Results: OECM-1 cells were subjected to short-term (10 minutes) or long-term (24 hours) BQE treatment
    (designated as SBT and LBT, respectively), and we found that both treatments increased MMP-2 protein and extracellular
    signal-regulated kinase (ERK) phosphorylation levels in a concentration- and time-dependent manner.
    LBT also increased MMP-2 mRNA level. LBT-induced MMP-2 secretion was not inhibited by PD98059 (up
    to 50 μM) when ERK was effectively blocked, but was attenuated by LY294002 (0–10 μM) in a concentrationdependent
    manner. This LBT effect was inhibited strongly by SB203580 (10 μM), SP600125 (10 μM), and
    Bay 11-7082 (10 μM) and mildly by N-acetyl-L-cysteine (5 mM), but not by U0126 (10 μM).
    Conclusion: Both SBT and LBT upregulate MMP-2 expression, and LBT-induced MMP-2 expression might be
    mediated by phosphoinositide 3-kinase, p38 mitogen-activated protein kinase, c-Jun N-terminal kinase,
    and nuclear factor-κB, and to a lesser extent, by reactive oxygen species, rather than by ERK.
    關聯: Journal of the Formosan Medical Association 109(11):p.838-847
    显示于类别:[生物科技系(所)] 期刊論文

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