篇名 | Studies on the Inhibitory Mechanisms of Baicalein in B16F10 Melanoma Cell Proliferation |
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卷期 | 19:3 |
作者 | Wen-Hsien Hsu 、 Wei-Wen Chang 、 Joen-RONG sHEU 、 Yu-Kai Hsiao 、 Yan-Jyu Tsai 、 Duen-Suey Chou |
頁次 | 331-339 |
關鍵字 | baicalein 、 12-lipoxygenase 、 reactive oxygen species 、 B16F10 cells 、 apoptosis 、 necrosis 、 MEDLINE 、 Scopus 、 SCIE |
出刊日期 | 201109 |
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.