篇名 | Gingernone A藉由增加細胞內活性氧物種生成及粒線體細胞凋亡路徑誘發SK-Hep-1細胞凋亡 |
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卷期 | 47 |
並列篇名 | Gingernone A-induced Apoptosis in SK-Hep-1 Cells is Mediated Via Increased Reactive Oxygen Species (ROS) Production and the Mitochondria-Associated Apoptotic Mechanisms |
作者 | 滿庭芳 、 陳中一 、 陳志良 、 劉崇喜 、 尹順君 |
頁次 | 001-014 |
關鍵字 | 生薑 、 細胞凋亡 、 活性氧 、 Ginger 、 apoptosis 、 reactive oxygen species |
出刊日期 | 201509 |
使用天然物來預防癌症發被認為是極具潛力的方式,本研究發現gingerenone A會透過誘發細胞凋亡進而抑制細胞生長,在細胞凋亡路徑探討方面,我們以外部路徑抑制劑(NOK-1, DR5 chimeric protein, and Etanercept)前處理細胞,發現並不能抑制gingerenone A誘發的細胞凋亡,關於粒線體調控的路徑方面,實驗結果發現gingerenone A會增加細胞內活性氧生成,降低粒線體膜電位及釋放cytochrome c至細胞質內,進而引發細胞凋亡,綜合上述,本研究結果顯示gingerenone A會藉由增加細胞內活性氧產生,活化粒線體調控的細胞凋亡路徑,導致細胞凋亡。
Chemoprevention by the use of naturally occurring substances is becoming a promising strategy to prevent cancer. In this study, gingernone A (Gin A) was found to elicit a concentration-dependent growth impediment. The demise of these cells induced by Gin A was apoptotic in nature, exhibiting a concentration-dependent increase in sub G1 fraction. In order to clarify whether death receptor-mediated pathways were involved in Gin A-induced apoptosis, the inhibitory effects of NOK-1, DR5 chimeric protein, and Etanercept on Gin A-induced apoptosis were examined. The results showed that these inhibitors could not prevent cells from becoming apoptosis-prone. As to the role of mitochondria in Gin A-induced apoptosis, we found that Gin A-treated cells displayed transient increase of ROS during the earlier stage of the experiment, followed by the disruption of mitochondrial transmembrane potential (ΔΨm). Subcellular fractionation analysis further revealed a rapid increase of cytochrome c in cytoplasm. Taken together, our data suggest that ROS plays an essential role in Gin A-induced apoptosis via mitochondrial pathways.