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題名 | Studies on the Inhibitory Mechanisms of Baicalein in B16F10 Melanoma Cell Proliferation=黃芩素對B16F10老鼠黑瘤細胞增生的抑制機轉之研究 |
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作者姓名(中文) | 許文憲; 張渭文; 許準榕; 蕭宇凱; 蔡妍菊; 周敦穗; | 書刊名 | Journal of Food and Drug Analysis |
卷期 | 19:3 2011.09[民100.09] |
頁次 | 頁331-339+379 |
分類號 | 414.33 |
關鍵詞 | 黃芩素; 12-脂加氧酶; 活性氧化物; B16F10細胞; 凋亡; 壞死; Baicalein; 12-lipoxygenase; Reactive oxygen species; B16F10 cells; Apoptosis; Necrosis; |
語文 | 英文(English) |
英文摘要 | ABSTRACT Baicalein induces the formation of superoxide and hydroxyl radicals via 12-lipoxygenase (12-LOX) in the B16F10 mouse melanoma cell line; baicalein also causes a reduction in cellular viability and induces cell apoptosis. In this study, we utilized ROS scavengers to evaluate the role of ROS in baicalein-induced cell death and used the 12-LOX downstream product, 12-hydroxyeicosatetraenoic acid (12-HETE), to counterbalance the 12-LOX-inhibitory action of baicalein. ROS scavengers had no effect on cell differentiation, but in the cellular viability (MTT) assay, ROS scavengers effectively reversed cell viability reduction induced by baicalein. A Western blot analysis revealed that the ROS scavengers had no effect on the cell apoptosis protein, active caspase-3. From the aspect of 12-LOX, 12-HETE had no effect on cell differentiation, but it effectively reversed the reduction in cellular viability caused by baicalein in B16F10 cells. 12-HETE also possessed an inhibitory effect on the increase in expression of active caspase-3 caused by baicalein. Combined pretreatment with ROS scavengers and 12-HETE minimized the damage caused by baicalein. The majority of cell death occurring in response to baicalein-induced ROS formation in B16F10 mouse melanoma was due to cell necrosis. Cell apoptosis due to 12-LOX suppression by baicalein only accounted for a small portion. |
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