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白花蛇舌草熊果酸诱导白血病耐药K562/ADM细胞凋亡及其作用机理的研究 被引量:18

Experimental Study on Apoptosis of Drug - Resistant Leukemia K562/ADM Cells Induced by Ursolic Acid Extract from Hedyotic Diffusa and Its Mechanisms
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摘要 目的:观察白花蛇舌草熊果酸(UAHD)对K562/ADM细胞株的生长抑制作用及诱导凋亡情况。方法:MTT法观察UAHD对K562/ADM细胞增殖抑制作用;光学显微镜观察药物作用后白血病细胞的形态学变化,琼脂糖凝胶电泳测定DNA梯状带,流式细胞仪测定药物对细胞的凋亡作用,检测GSH、GST、GSH-PX、MDA探讨凋亡相关机制。结果:UAHD作用于K562/ADM细胞24 h抑制率为:7.2%、10.6%、16.0%、75.6%;48 h抑制率为:33%、39%、51.1%、61.6%,72 h抑制率为:34.1%、52.2%、72.7%、64.9%。UAHD作用K562/ADM细胞48 h细胞凋亡率分别为:3.18%、8.78%、17.83%、23.52%。结论:UAHD能够诱导K562/ADM细胞凋亡,凋亡的机制与细胞内氧化应激反应有关。 Objective:To observe the inhibition and apoptosis about K562/ADM cells induced by ursolic acid extracts from Hedyotis diffusa Willd (UAHD). Methods:MTT colorimetric assay was used to examine the growth inhibition on leu- kemia K562/ADM cell by UAHD, observing the cell morphological change on the kind of cell by the various concentra- tions of the extraction by light microscope. DNA ladder was analyzed respectively by DNA agarose gel electrophoresis. The apoptosis rate was analyzed by Annexin V/PI flow cytometry. The glutathione( GSH)level and activity of glutathione S- transferase (GST), glutathione peroxidase (GPX)and lipid peroxidation (MDA)level in the K562/ADM cells were tested to explore the mechanisms. Results:Exposure of K562/ADM cells treated with definite concentration of UAHD for 24 hours,and the inhibition rates were 7.2%, 10.6% , 16.0% and 75.6% respectively,for 48 h, the inhibition rates were 33% ,39% ,51.1% and 61.6% ;for 72 h,the inhibition rates were 34.1% ,52.2% ,72.7% and 64.9%. The apoptosis rates were analyzed by Annexin V/PI flow cytometry,showing the apoptosis rates of 48 h were 3.18% ,8.78%, 17.83% and 23.52%, Conclusion:UAHD induces apoptosis in human leukemia K562/ADM cells,and the mechanisms are associ- ated with mitochondrial signaling pathway.
出处 《中华中医药学刊》 CAS 2013年第4期921-924,I0013,共5页 Chinese Archives of Traditional Chinese Medicine
关键词 白花蛇舌草 熊果酸 白血病 耐药 凋亡 氧化 线粒体 Hedyotis diffusa ursolic acid leukemia multidrug resistant apoptosis oxidation mitochondria
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