中國醫藥大學機構典藏 China Medical University Repository, Taiwan:Item 310903500/28667
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    請使用永久網址來引用或連結此文件: http://ir.cmu.edu.tw/ir/handle/310903500/28667


    題名: Increase of anti-oxidation by exercise in the liver of obese Zucker rats
    作者: Chang, SP;Chen, YH;Chang, WC;Liu, IM;Cheng, JT
    貢獻者: 中國醫藥大學;Natl Cheng Kung Univ, Coll Med, Dept Pharmacol, Tainan 70101, Taiwan;China Med Univ, Chung Tai Inst Hlth Sci & Technol, Taichung, Taiwan;China Med Univ, Dept Sports Med, Taichung, Taiwan;Natl Cheng Kung Univ, Tajen Inst Technol, Tainan, Taiwan
    日期: 2004
    上傳時間: 2010-09-24 13:39:41 (UTC+8)
    出版者: BLACKWELL PUBLISHING ASIA
    摘要: Genistein, an isoflavonoid natural product, is widely used to inhibit protein tyrosine kinase (PTK). In the present study, we investigated the possible influence of genistein on alpha(1)-adrenoceptors (AR) in cultured C2C12 cells. Genistein enhanced the uptake of radioactive glucose into C2C12 cells in a concentration-dependent manner. Similar results were also observed in samples treated with daidzein, the inactive congener for PTK inhibition. The effect of genistein on alpha(1)-AR was further characterized using the displacement of [H-3]prazosin binding in C2C12 cells. The increase in radioactive glucose uptake by genistein was abolished by RS17053 at a concentration sufficient to block alpha(1A)-AR. The pharmacological inhibition of phospholipase C (PLC) by U73122 resulted in a concentration-dependent reduction of genistein-stimulated glucose uptake in C2C12 cells. This inhibition by U73122 was specific because the inactive congener, U73343, failed to modify the action of genistein. Moreover, genistein can activate alpha(1A)-AR at a concentration (I mumol/L) lower than that (50 mumol/L) needed to abolish the insulin-stimulated phosphorylation of PTK. The obtained data indicate an activation Of alpha(1A)-AR by genistein to increase the glucose uptake into C2C12 cells and this supports the application of genistein as a TK inhibitor.
    關聯: CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY 31(8):506-511
    顯示於類別:[中國醫藥大學] 期刊論文

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