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http://asiair.asia.edu.tw/ir/handle/310904400/17330
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Title: | Pipoxolan inhibits proliferation of HL-60 human leukaemia cancer cells by arresting the cell cycle at the G0?G1 phase |
Authors: | Sheu, Ming-Jyh;Chou, Pei-Yu;Huang, Chin-Shiu3
Tsai, I-Chun;Chien, Yi-Chung;Lin, Sung-Yuan;Tsai, Huei-Yann;Cheng, Hsu-Chen;Wu, Chieh-Hsi |
Contributors: | 保健營養生技學系 |
Keywords: | anti-proliferation;apoptosis;caspase 3;pipoxolan;reactive oxygen species. |
Date: | 2010-01 |
Issue Date: | 2012-11-26 02:31:35 (UTC+0) |
Abstract: | 1. The aim of the present study was to investigate the molecular mechanisms by which pipoxolan exerts its inhibitory effects and apoptotic activity in human leukaemia HL-60 cells. 2. The effects of pipoxolan on the proliferation of HL-60 cells and on the distribution of cells within different phases of the cell cycle were investigated indirectly using a Trypan blue assay and a flow cytometer, respectively. The effects of pipoxolan on the apoptosis of HL-60 cells was investigated using DNA fragmentation and flow cytometer. The expression of factors affecting the cell cycle and apoptosis, including p53, p21, Bax, Bcl2, cytochrome c, caspase 3 and caspase 9, was examined by western blotting. 3. At 6.25 μg/mL, pipoxolan significantly induced apoptosis in human leukaemia HL-60 cells after 24 h exposure. In addition, HL-60 cells were arrested in the G0/G1 phase via the induction of p53/p21 by pipoxolan. Apoptosis was associated with an increased Bax/Bcl-2 ratio, cytochrome c release, cleavage of procaspases-9 and -3 and hydrolysis of poly(ADP-ribose) polymerase. Intracellular reactive oxygen species (ROS) seem to play a key role in the pipoxolan-induced apoptosis, because high levels of ROS were produced early in the drug treatment. Apoptosis was significantly abrogated by the free radical scavenger N-acetylcysteine (NAC). |
Relation: | CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, 37(5/6):605-612. |
Appears in Collections: | [食品營養與保健生技學系] 期刊論文
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