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机构地区:[1]武汉科技大学医学院附属医院内科,湖北武汉430080
出 处:《中国现代医学杂志》2006年第11期1642-1645,共4页China Journal of Modern Medicine
摘 要:目的研究表明组蛋白去乙酰化酶(histonedeacetylase,HDAC1)在多种肿瘤中高表达,曲古菌素A(trichostatinA,TSA)可以抑制肿瘤细胞的生长。该实验研究HDAC1在K562细胞的表达及TSA对其增殖的影响。方法50~400nmol/L的TSA分别处理K562细胞8~48h后用四甲基偶氮唑蓝(MTT法)比色检测K562细胞的生长活性;应用流式细胞仪法观察细胞凋亡。RT-PCR和蛋白印迹法(westernblot)方法检测K562细胞在24h不同浓度(50~400nmol/L)的条件下HDAC1的mRNA和蛋白的表达以及TSA对其作用。结果TSA可显著抑制K562细胞的生长,诱导细胞发生凋亡,并呈时间及剂量依赖性。HDAC1的mRNAA值的半定量表达以及蛋白表达明显增强(P<0.05),但随着浓度的增加而表达下调。结论TSA对K562细胞具有明显的增生抑制及诱导凋亡作用,抑制HDAC1的表达,可能是其重要作用机制之一。[Objective] It was manifested that Histone Deacetylase(HDAC1) was expressed highly in many kinds of the tumor cells, and Trichostatin A(TSA) could inhibit their growth. The aim of this experiment was to research the expression of HDAC1 in K562 ceils and the influence of TSA on their proliferation. [Method] K562 cells were treated with TSA in concentrations from 50 to 400 nmol/L for 8 to 48 hours. Then the growth activity was assayed by Dipenyhetrazolium bromide (MTt) colorimetric assay. The apoptosis of cells were observed by flow cytometery(FCM). The mRNA and protein's expressions of K562 ceils, which were treated with HDAC1 in various concentrations from 50 to 400 nmol/L for 24 hours, were determined by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot analysis. Further more; the effect of TSA on them was assayed in the same way.[Results] TSA can inhibit the growth of K562 cells and induce the apoptosis of the ceils remarkably, and they were in a time-and-dosedependent manner. The protein expression and the mRNA semiquantitative expression of HDAC1 were enhanced obviously (P 〈0.05), but the expressions were down-regulated with the increase of the concentrations. [Conclusion] TSA can inhibit the proliferation of K562 cells and induce their apoptosis remarkably. One of their important mech- anisms probably is that it can inhibit the expression of HDAC1.
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