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    題名: Diallyl disulfide induces apoptosis in human colon cancer cell line (COLO 205) through the induction of reactive oxygen species, endoplasmic reticulum stress, caspases casade and mitochondrial-dependent pathways.
    作者: 楊家欣(Yang Jai-Sing);陳光偉(Guang-Wei Chen);夏德椿(Te-Chun Hsia);何恆堅(Heng-Chien Ho);何蓁蓁(Chin-Chin Ho);(Meng-Wei Lin);林松水(Song-Shei Lin);(Ru-Duan Yeh);葉兆雲(Ip Siu-Wan);(Hsu-Fung Lu);鍾景光(Jing-Gung Chung)*
    貢獻者: 醫學院醫學系學士班藥理學科
    關鍵詞: Diallyl disulfide;Caspase-3;Apoptosis;Mitochondria;Reactive oxygen species;cDNA microarray
    日期: 2009-01
    上傳時間: 2009-08-19 17:23:59 (UTC+8)
    摘要: In this study, we investigated the effects of DADS on human colon cancer cell line COLO 205 on cell cycle arrest and apoptosis in vitro. After 24 h treatment of COLO 205 cells with DADS, the dose- and time-dependent decreases of viable cells were observed and the IC50 was 22.47 μM. The decreased percentages of viable cells are associated with the production of ROS. Treatment of COLO 205 cells with DADS resulted in G2/M phase arrest and apoptosis occurrence through the mitochondrial-pathway (Bcl-2, Bcl-xL down-regulation and Bak, Bax up-regulation). DADS increased cyclin B, cdc25c-ser-216-9 and Wee1 but did not affect CDK1 protein and gene expression within 24 h of treatment. DADS-induced apoptosis was examined and confirmed by DAPI staining and DNA fragmentation assay. DADS promoted caspase-3, -8 and -9 activity and induced apoptosis were accompanied by increasing the levels of Fas, phospho-Ask1 and -JNK, p53 and decreasing the mitochondrial membrane potential which then led to release the cytochrome c, cleavage of pro-caspase-9 and -3. The COLO 205 cells were pre-treated with JNK inhibitor before leading to decrease the percentage of apoptosis which was induced by DADS. Inhibition of caspase-3 activation blocked DADS-induced apoptosis on COLO 205 cells.
    關聯: FOOD AND CHEMICAL TOXICOLOGY 47(1):171~179
    顯示於類別:[醫學系] 期刊論文

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