Involvement of Bax, Bcl-2, Ca2+ and Caspase-3 in Capsaicin-induced Apoptosis of Human Leukemia HL-60 Cells

中國醫藥大學機構典藏 China Medical University Repository, Taiwan > 台中附設醫院 > 期刊論文 > Item 310903500/2617

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题名:	Involvement of Bax, Bcl-2, Ca2+ and Caspase-3 in Capsaicin-induced Apoptosis of Human Leukemia HL-60 Cells
作者:	鄒梅芬(Tsou Mei-Fen);呂旭峰(Lu Hsu-Feng);蘇進成(Chen Ssu-Ching);吳禮字(Wu Lii-Tzu);陳怡璇(Chen Yi-Shuan);郭秀滿(Kuo Hsiu-Maan);林松水(Lin Song-Shei);鍾景光(Chung Jing-Gung)
贡献者:	中國附醫檢驗醫學部生化組
关键词:	Capsaicin;cell cycle;apoptosis;calcium;HL-60
日期:	2006-05
上传时间:	2009-08-20 17:32:15 (UTC+8)
摘要:	The role of Ca2+ on the effects of capsaicin on human leukemia HL-60 cells in vitro and the molecular mechanisms of capsaicin-induced apoptosis were investigated. The flow cytometric analysis indicated that capsaicin decreased the percentage of viable HL-60 cells, via the induction of G0/G1-phase cell cycle arrest and apoptosis. Capsaicin-induced G0/G1-phase arrest involved the suppression of CDK2 and the cyclin E complex, which are check-point enzymes for cells moving from G0/G1- to S-phase. Capsaicin-induced apoptosis was associated with the elevation of intracellular reactive oxygen species and Ca2+ production, decreased the levels of mitochondrial membrane potential, promoted cytochrome c release and increased the activation of caspase-3. An intracellular Ca2+ chelator (BAPTA) significantly inhibited capsaicin-induced apoptosis. Capsaicin-induced apoptosis was time-and dose-dependent. These results suggest that the capsaicin-induced apoptosis of HL-60 cells may result from the activation of caspase-3 and the intracellular Ca2+ release pathway.
關聯:	ANTICANCER RESEARCH 26(3A):1965~1972
显示于类别:	[台中附設醫院] 期刊論文

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