 |
English
|
正體中文
|
简体中文
|
全文筆數/總筆數 : 18076/20274 (89%)
造訪人次 : 5250955
線上人數 : 1177
|
|
|
資料載入中.....
|
請使用永久網址來引用或連結此文件:
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 |
| 顯示於類別: | [生物科技系(所)] 期刊論文
|
文件中的檔案:
| 檔案 |
描述 |
大小 | 格式 | 瀏覽次數 |
|---|
| index.html | | 0Kb | HTML | 2345 | 檢視/開啟 |
|
在CNU IR中所有的資料項目都受到原著作權保護.
|
