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作 者:姚丽[1] 何敬和[1] 谢红[1] 呼文亮[1] 陈立军[1]
机构地区:[1]中国人民武装警察部队医学院基础部生化教研室,天津300162
出 处:《中华中医药杂志》2009年第12期1586-1589,共4页China Journal of Traditional Chinese Medicine and Pharmacy
基 金:天津市科委课题资助项目(No.05YFJMJC08200)
摘 要:目的:基因芯片检测青蒿素及其衍生物(青蒿琥酯和二氢青蒿素)作用于K562细胞后的基因表达情况,从基因水平上探讨青蒿素及其衍生物抑制K562增殖的作用机制;方法:药物处理K562细胞,倒置光显微镜和荧光显微镜观察细胞形态学,流式细胞仪检测细胞周期。MTT检测细胞生长抑制率。基因芯片检测基因表达;结果:倒置光显微镜:细胞核分裂相减少,细胞密度下降。荧光显微镜:细胞有明显的染色质凝集。流式细胞仪:G2期细胞的比例增加。MTT:药物抑制K562细胞生长。芯片杂交数据分析,青蒿素组有10条基因表达下调,青蒿琥酯组10条基因表达有差异,二氢青蒿素组13条基因表达有差异;结论:青蒿素及其衍生物可抑制K562细胞增殖,作用机制与改变细胞周期某些调控物质的基因表达、诱导K562细胞凋亡等有关。Objective:In order to understanding how Artemisinin and its derivatives(artesunate and dihydroartemisinin )inhibited leukaemia cell line K562,on the molecular level,the gene chip was used to detect the expression panel ofgenes ofleukaemia cell line K562 treated by Artesunate.Methods:K562 cells were treated with Artemisinin and its derivatives for 24h,and then studied modality changes under invert microscope.The morphology changes ofthe nucleons were observed by Hoechst33342/PI staining.The cell cycle state was examined by flow cytometry analysis.Inhibitory rate ofdrugs to K562 cells was determined by MTT.Total RNA samplesobtained by TRIzol and were reverse transcribed to the cDNA.cDNA samples were hybridized to gene chips.Hybridization signal were collected and analyzed following scanning by Gene Pix 4100A.Results:The numbers ofdrift cells increased and the density ofcells decreased under invert microscope after K562 cells were treated by Artesunate for 24h.Morphology changes ofcell apoptosis such as karyopyknosis and conglomeration were observed by Hoechst33342/PI staining.Flow cytometric analysisshowed that cells were arrested in G2 phase.Drugs could inhibit proliferation ofK562.Hybridization analysis showed 10 pieces genes expression were regulated down in the Artemisinin-treated K562 cells, 13 pieces genes expression were different in the dihydroartemisinin-treated K562 cells,10 pieces genes expression were different in the Artesunate-treated K562 cells.Conclusion:Artemisinin and its derivatives could inhibite the proliferation ofleukaemia cell line K562, and the mechanism may be correlated with altering the expression ofthese genes involved in cell cycle and inducing k562 apoptosis.
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