白血病·淋巴瘤
白血病·淋巴瘤
백혈병·림파류
JOURNAL OF LEUKEMIA & LYMPHOMA
2011年
5期
275-277,281
,共4页
肿瘤,实验性%白血病%地西他滨%三氧化二砷%NB4细胞%细胞凋亡
腫瘤,實驗性%白血病%地西他濱%三氧化二砷%NB4細胞%細胞凋亡
종류,실험성%백혈병%지서타빈%삼양화이신%NB4세포%세포조망
Neoplasms,experimental%Leukemia%Decitabine%As2O3%NB4 cells%Apoptosis
目的 研究去甲基化制剂地西他滨(DAC)单用或联合三氧化二砷(As2O3)对NB4细胞凋亡的作用机制.方法 将不同浓度的DAC、As2O3以及两药联合作用于NB4细胞,不加药为对照组,采用四甲基偶氮唑蓝(MTT)法检测细胞增殖抑制作用,流式细胞术检测细胞凋亡.结果 DAC与As2O3单药对NB4细胞的抑制作用呈浓度时间依赖性(DAC 1 μmol/L作用24、48、72 h的抑制率分别为12.18%、22.72%、35.54%;DAC 2 μmol/L作用24、48、72 h的抑制率分别增高为22.14%、31.18%、45.21%;As2O3 0.5 μmol/L作用24、48、72 h的抑制率分别21.09%、32.43%、44.93%;As2O3 1.0 μmol/L作用24、48、72 h的抑制率分别增高为31.69%、41.12%及54.27%),两药联合抑制作用较单药明显(DAC 1 μmol/L+As2O3 0.5 μmol/L作用24、48、72 h抑制率分别为42.10%、48.75%、60.78%)(P<0.05),各浓度组与对照组比较差异均有统计学意义(P值均<0.05);As2O3 1 μmol/L作用于NB4细胞株48 h可见5.8%的细胞凋亡,联合组增高为17.3%.结论 DAC能显著抑制NB4细胞的增殖并诱导其凋亡,DAC联合As2O3对NB4细胞增殖抑制及诱导凋亡有协同作用.
目的 研究去甲基化製劑地西他濱(DAC)單用或聯閤三氧化二砷(As2O3)對NB4細胞凋亡的作用機製.方法 將不同濃度的DAC、As2O3以及兩藥聯閤作用于NB4細胞,不加藥為對照組,採用四甲基偶氮唑藍(MTT)法檢測細胞增殖抑製作用,流式細胞術檢測細胞凋亡.結果 DAC與As2O3單藥對NB4細胞的抑製作用呈濃度時間依賴性(DAC 1 μmol/L作用24、48、72 h的抑製率分彆為12.18%、22.72%、35.54%;DAC 2 μmol/L作用24、48、72 h的抑製率分彆增高為22.14%、31.18%、45.21%;As2O3 0.5 μmol/L作用24、48、72 h的抑製率分彆21.09%、32.43%、44.93%;As2O3 1.0 μmol/L作用24、48、72 h的抑製率分彆增高為31.69%、41.12%及54.27%),兩藥聯閤抑製作用較單藥明顯(DAC 1 μmol/L+As2O3 0.5 μmol/L作用24、48、72 h抑製率分彆為42.10%、48.75%、60.78%)(P<0.05),各濃度組與對照組比較差異均有統計學意義(P值均<0.05);As2O3 1 μmol/L作用于NB4細胞株48 h可見5.8%的細胞凋亡,聯閤組增高為17.3%.結論 DAC能顯著抑製NB4細胞的增殖併誘導其凋亡,DAC聯閤As2O3對NB4細胞增殖抑製及誘導凋亡有協同作用.
목적 연구거갑기화제제지서타빈(DAC)단용혹연합삼양화이신(As2O3)대NB4세포조망적작용궤제.방법 장불동농도적DAC、As2O3이급량약연합작용우NB4세포,불가약위대조조,채용사갑기우담서람(MTT)법검측세포증식억제작용,류식세포술검측세포조망.결과 DAC여As2O3단약대NB4세포적억제작용정농도시간의뢰성(DAC 1 μmol/L작용24、48、72 h적억제솔분별위12.18%、22.72%、35.54%;DAC 2 μmol/L작용24、48、72 h적억제솔분별증고위22.14%、31.18%、45.21%;As2O3 0.5 μmol/L작용24、48、72 h적억제솔분별21.09%、32.43%、44.93%;As2O3 1.0 μmol/L작용24、48、72 h적억제솔분별증고위31.69%、41.12%급54.27%),량약연합억제작용교단약명현(DAC 1 μmol/L+As2O3 0.5 μmol/L작용24、48、72 h억제솔분별위42.10%、48.75%、60.78%)(P<0.05),각농도조여대조조비교차이균유통계학의의(P치균<0.05);As2O3 1 μmol/L작용우NB4세포주48 h가견5.8%적세포조망,연합조증고위17.3%.결론 DAC능현저억제NB4세포적증식병유도기조망,DAC연합As2O3대NB4세포증식억제급유도조망유협동작용.
Objective To investigate the effect of methylation inhibitor decitabine (DAC) alone and combination with As2O3 on apoptosis of NB4 cells. Methods NB4 cells were treated with DAC, As2O3 and the combination of them in different concentrations. The cell proliferation was analyzed by MTT assay and the apoptosis of NB4 cells was detected by flow cytometry. Results Both DAC and As2O3 induced time and concentration-dependent cell death, in which the inhabitation rate were 12.18 %, 22.72 %, 35.54 %, respectively, after 24 h, 48 h, 72 h on treatment by DAC at 1 μmol/L and the inhibition rates were increased to 22.14 %, 31.18 %, 45.21 % by DAC at 1 μmol/L. The inhibition rates were 21.09 %, 32.43 %, 44.93 %, respectively, by treating with As2O3 0.5 μmol/L after 24 h, 48 h, 72 h, which were increased to 31.69 %, 41.12 % and 54.27 %, respectively after 24 h, 48 h, 72 h. The inhibition rates were significantly increased by using both DAC and As2O3 with significant differences (P <0.05). DAC and As2O3 in combination produced a greater inhibition of growth against NB4 cells (by treating with DAC 1 μmol/L + As2O3 0.5 μmol/L after 24 h, 48 h, 72 h, the inhibition rates were 42.10 %, 48.75 %, 60.78 %) (P <0.05). In each concentration group and control group the differences were statistically significant (P <0.05). The incubation for 48 h with As2O3 1 μmol/L alone or combined with DAC 2 μmol/L showed apoptosis cells by 5.8 % and 17.3 %. Conclusion Decitabine can significantly inhibit the proliferation of NB4 cells and the apoptosis with synergistic effectiveness can be found when Decitabine combination with As2O3.
