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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/310903500/30305
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題名: | Emodin induces apoptosis in human lung adenocarcinoma cells through a reactive oxygen species-dependent mitochondrial signaling pathway |
作者: | Su, YT;Chang, HL;Shyue, SK;Hsu, SL |
貢獻者: | 醫學院醫研所;Taichung Vet Gen Hosp, Dept Educ & Res, Taichung, Taiwan;China Med Univ, Inst Med Sci, Taichung, Taiwan;China Med Univ, Sch Med, Taichung, Taiwan;Acad Sinica, Inst Biomed Sci, Taipei, Taiwan;Chung Shan Med Univ, Inst Toxicol, Taichung, Taiwan;China Med Univ, Inst Chinese Pharmaceut Sci, Taichung, Taiwan |
日期: | 2005 |
上傳時間: | 2010-09-24 14:52:54 (UTC+8) |
出版者: | PERGAMON-ELSEVIER SCIENCE LTD |
摘要: | N-acetyltransferases (NATs) are recognized to play a key role in the primary step of arylamine compounds metabolism. Polymorphic NAT is coded for rapid or slow acetylators, which are being thought to involve cancer risk related to environmental exposure. Berberine has been shown to induce apoptosis and affect NAT activity in human leukemia cells. The purpose of this study is to examine whether or not berberine could affect arylamine NAT activity and gene expression (NAT mRNA) and the levels of NAT protein in mouse leukemia cells (L 1210). N-acetylated and non-N-acetylated AF were determined and quantited by using high performance liquid chromatography. NAT mRNA was determined and quantited by using RT-PCR. The levels of NAT protein were examined by western blotting and determined by using flow cytometry. Berberine displayed a dose-dependent inhibition to cytosolic NAT activity and intact mice leukemia cells. Time-course experiments indicated that N-acetylation of AF measured from intact mice leukemia cells were inhibited by berberine for up to 24h. The NAT1 mRNA and NAT proteins in mouse leukemia cells were also inhibited by berberine. This report is the first demonstration, which showed berberine affect mice leukemia cells NAT activity, gene expression (NAT1 mRNA) and levels of NAT protein. (c) 2005 Published by Elsevier GrnbH. |
關聯: | BIOCHEMICAL PHARMACOLOGY 70(2):229-241 |
顯示於類別: | [醫學研究所] 期刊論文
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