活性氧通过Gadd153的表达和线粒体依赖性途径介导黄芩苷诱导人早幼粒细胞白血病HL-60细胞凋亡。
ROS mediates baicalin-induced apoptosis in human promyelocytic leukemia HL-60 cells through the expression of the Gadd153 and mitochondrial-dependent pathway.
作者信息
Lu Hsu-Fung, Hsueh Shu-Ching, Ho Yung-Tsuan, Kao Ming-Ching, Yang Jai-Sing, Chiu Tsan-Hung, Huamg Shau-Yen, Lin Ching-Chung, Chung Jing-Gung
机构信息
Department of Clinical Pathology, Cheng Hsin Rehabilitation Medical Center, Taipei, Taiwan, ROC.
出版信息
Anticancer Res. 2007 Jan-Feb;27(1A):117-25.
BACKGROUND
Chemotherapy agents, particularly those that can induce apoptosis, are the major intervening strategy in the treatment of leukemia. In this study, we investigated the effects of baicalin (a compound obtained from Scutellaria baicalensis Georgi and S. rivularis Benth Labiateae) on the viability, induction of apoptosis and associated mechanism in human leukemia HL-60 cells.
MATERIALS AND METHODS
The cell viability and apoptosis was examined by flow cytometric analysis. The results showed that baicalin induced cytotoxicity in a dose- and time-dependent manner through the activation of caspase-3, as shown by treatment of HL-60 cells with an inhibitor of caspase-3 (z-VAD-fmk). Baicalin increased the levels of ROS, Ca2+ and decreased mitochondrial membrane potential in HL-60 cells. Western blot demonstrated that baicalin promoted the levels of Gadd153, Bax, cytochrome c and caspase-3 and -12, but decreased the levels of Grp78 and Bcl-2 in HL-60 cells.
CONCLUSION
Baicalin was found to induce apoptosis in HL-60 cells through multiple pathways.
背景
化疗药物，尤其是那些能够诱导细胞凋亡的药物，是白血病治疗中的主要干预策略。在本研究中，我们调查了黄芩苷（一种从唇形科植物黄芩和溪黄草中提取的化合物）对人白血病HL-60细胞活力、凋亡诱导及相关机制的影响。
材料与方法
通过流式细胞术分析检测细胞活力和凋亡情况。结果显示，黄芩苷通过激活半胱天冬酶-3以剂量和时间依赖性方式诱导细胞毒性，这通过用半胱天冬酶-3抑制剂（z-VAD-fmk）处理HL-60细胞得以证明。黄芩苷增加了HL-60细胞中活性氧（ROS）、钙离子（Ca2+）水平，并降低了线粒体膜电位。蛋白质免疫印迹法表明，黄芩苷促进了HL-60细胞中Gadd153、Bax、细胞色素c以及半胱天冬酶-3和-12的水平，但降低了Grp78和Bcl-2的水平。
结论
发现黄芩苷通过多种途径诱导HL-60细胞凋亡。
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