Arecoline-mediated inhibition of AMP-activated protein kinase through reactive oxygen species is required for apoptosis induction

doi:10.1016/j.oraloncology.2011.02.014

Chia Nan University of Pharmacy & Science Institutional Repository > 藥理學院 > 生物科技系(所) > 期刊論文 > Item 310902800/26689

Please use this identifier to cite or link to this item: https://ir.cnu.edu.tw/handle/310902800/26689

標題:	Arecoline-mediated inhibition of AMP-activated protein kinase through reactive oxygen species is required for apoptosis induction
作者:	Yen, Ching-Yu Lin, Mei-Huei Liu, Shyun-Yeu Chiang, Wei-Fan Hsieh, Wan-Fang Cheng, Yon-Chi Hsu, Kai-Cheng Liu, Young-Chau
貢獻者:	生物科技系
關鍵字:	Areca nut;Arecoline ROS AMPK Apoptosis
日期:	2011-05
上傳時間:	2013-06-05 16:42:45 (UTC+8)
出版者:	Elsevier Elsevier
摘要:	Arecoline is the major alkaloid of areca nut (AN) and known to induce reactive oxygen species (ROS) production and apoptosis. The metabolic sensor AMP-activated protein kinase (AMPK), activated by ROS, also regulates apoptosis. This study used several types of cells as the experimental model to analyze the roles of ROS and AMPK in arecoline-induced apoptosis. We found that arecoline dose-dependently increased intracellular ROS level, and two antioxidants, N-acetyl-l-cysteine (NAC) and glutathione, attenuated arecoline-induced apoptotic cell death. Interestingly, arecoline dose- and time-dependently inhibited rather than stimulated AMPK-Thr172 phosphorylation, and both NAC and glutathione relieved this inhibition. The AMPK activator, 5-aminoimidazole-4-carboxamide 1-β-D-ribofuranoside (AICAR), also restored the phosphorylation level of AMPK-Thr172 and attenuated apoptotic cell death under arecoline insult. In contrast, the AMPK inhibitor, compound C, and RNA interference of AMPK expression increased the cytotoxicity of arecoline. Collectively, these results suggest that arecoline may inhibit AMPK through intracellular ROS, responsible for the execution of apoptosis.
關聯:	Oral oncology 47(5), pp.345-351
Appears in Collections:	[生物科技系(所)] 期刊論文

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