白血病·淋巴瘤
白血病·淋巴瘤
백혈병·림파류
JOURNAL OF LEUKEMIA & LYMPHOMA
2009年
6期
335-337,341
,共4页
韦苇%周帆%侯健%郭列平%张忆梓%杨盛玲
韋葦%週帆%侯健%郭列平%張憶梓%楊盛玲
위위%주범%후건%곽렬평%장억재%양성령
骨髓增生异常综合征%MUTZ-1细胞%三氧化二砷%沙利度胺%Bmi-1%基因
骨髓增生異常綜閤徵%MUTZ-1細胞%三氧化二砷%沙利度胺%Bmi-1%基因
골수증생이상종합정%MUTZ-1세포%삼양화이신%사리도알%Bmi-1%기인
Myelodysplastic syndrome%MUTZ-1 cells%Arsenic trioxide%Thalidomide%Bmi-1%Gene
目的 探讨沙利度胺和三氧化二砷对人类骨髓增生异常综合征细胞株MUTZ-1的影响及其作用机制.方法 采用CCK-8法检测三氧化二砷、沙利度胺以及二者联合用药对MUTZ-1细胞株增生是否有抑制作用.采用半定量RT-PCR方法分别检测三氧化二砷、沙利度胺以及二者联合对MUTZ-1的Bmi-1基因是否有抑制作用,并用流式细胞术对细胞株行凋亡检测.结果 沙利度胺体外对MUTZ-1细胞无明显生长抑制作用(P>0.05),三氧化二砷对MUTZ-1细胞有明显生长抑制作用(P<0.05),联合用药组的抑制作用明显高于三氧化二砷、沙利度胺单独用药组(CDI<0.7);三氧化二砷组的细胞凋亡率随着药物浓度增加而升高,呈剂量依赖(r=0.627,P<0.05);沙利度胺组细胞凋亡率随着药物浓度增加无明显升高(r=0.313,P>0.05),联合用药组随着药物浓度增加表达亦升高(P<0.05);三氧化二砷组Bmi-1/β-actin随着药物浓度增加表达下降,呈剂量依赖性(r=-0.912,P<0.05),沙利度胺组Bmi-1/β-actin随着药物浓度增加表达无明显下降(r=0.594,P>0.05),联合用药组对Bmi-1的抑制作用明显高于三氧化二砷、沙利度胺单独用药组(CDI<0.7).结论 沙利度胺体外对MUTZ-1细胞无明显生长抑制作用,三氧化二砷对MUTZ-1细胞有明显生长抑制作用,联合用药组的抑制作用明显提高.
目的 探討沙利度胺和三氧化二砷對人類骨髓增生異常綜閤徵細胞株MUTZ-1的影響及其作用機製.方法 採用CCK-8法檢測三氧化二砷、沙利度胺以及二者聯閤用藥對MUTZ-1細胞株增生是否有抑製作用.採用半定量RT-PCR方法分彆檢測三氧化二砷、沙利度胺以及二者聯閤對MUTZ-1的Bmi-1基因是否有抑製作用,併用流式細胞術對細胞株行凋亡檢測.結果 沙利度胺體外對MUTZ-1細胞無明顯生長抑製作用(P>0.05),三氧化二砷對MUTZ-1細胞有明顯生長抑製作用(P<0.05),聯閤用藥組的抑製作用明顯高于三氧化二砷、沙利度胺單獨用藥組(CDI<0.7);三氧化二砷組的細胞凋亡率隨著藥物濃度增加而升高,呈劑量依賴(r=0.627,P<0.05);沙利度胺組細胞凋亡率隨著藥物濃度增加無明顯升高(r=0.313,P>0.05),聯閤用藥組隨著藥物濃度增加錶達亦升高(P<0.05);三氧化二砷組Bmi-1/β-actin隨著藥物濃度增加錶達下降,呈劑量依賴性(r=-0.912,P<0.05),沙利度胺組Bmi-1/β-actin隨著藥物濃度增加錶達無明顯下降(r=0.594,P>0.05),聯閤用藥組對Bmi-1的抑製作用明顯高于三氧化二砷、沙利度胺單獨用藥組(CDI<0.7).結論 沙利度胺體外對MUTZ-1細胞無明顯生長抑製作用,三氧化二砷對MUTZ-1細胞有明顯生長抑製作用,聯閤用藥組的抑製作用明顯提高.
목적 탐토사리도알화삼양화이신대인류골수증생이상종합정세포주MUTZ-1적영향급기작용궤제.방법 채용CCK-8법검측삼양화이신、사리도알이급이자연합용약대MUTZ-1세포주증생시부유억제작용.채용반정량RT-PCR방법분별검측삼양화이신、사리도알이급이자연합대MUTZ-1적Bmi-1기인시부유억제작용,병용류식세포술대세포주행조망검측.결과 사리도알체외대MUTZ-1세포무명현생장억제작용(P>0.05),삼양화이신대MUTZ-1세포유명현생장억제작용(P<0.05),연합용약조적억제작용명현고우삼양화이신、사리도알단독용약조(CDI<0.7);삼양화이신조적세포조망솔수착약물농도증가이승고,정제량의뢰(r=0.627,P<0.05);사리도알조세포조망솔수착약물농도증가무명현승고(r=0.313,P>0.05),연합용약조수착약물농도증가표체역승고(P<0.05);삼양화이신조Bmi-1/β-actin수착약물농도증가표체하강,정제량의뢰성(r=-0.912,P<0.05),사리도알조Bmi-1/β-actin수착약물농도증가표체무명현하강(r=0.594,P>0.05),연합용약조대Bmi-1적억제작용명현고우삼양화이신、사리도알단독용약조(CDI<0.7).결론 사리도알체외대MUTZ-1세포무명현생장억제작용,삼양화이신대MUTZ-1세포유명현생장억제작용,연합용약조적억제작용명현제고.
Objective To study the effect of thalidomide and arsenic trioxide on the proliferation and apoptosis effect in human myelodysplastic syndrome cell line MUTZ-1 and explore its possible mechanism.Methods MUTZ-1 cells were cultured with different concentration of thalidomide alone, arsenic trioxide alone, and thalidomide plus arsenic trioxide for 48 h. The cell proliferation was analyzed by CCK-8 test, and cell apoptosis was analyzed by flow cytometry. The expression of Bmi-1 was analyzed by semi-quantitative RT-PCR. Results Thalidomide alone had no significant inhibition on growth of MUTZ-1 cells (P >0.05).Arsenic trioxide alone had obviously inhibited the cell proliferation (P <0.05). While thalidomide plus arsenic trioxide group had the great inhibition effect(CDI <0.7), and reveal was that two drugs had synergism effect on inhibiting the MUTZ-1 cells. Arsenic trioxide group of apoptosis rate was increased with higher concentrations of drug, a dose-dependent (r = 0.627, P <0.05), thalidomide in the rate of apoptosis with no increase in drug concentration significantly (r= 0.313, P> 0.05), and the combined group with the drug also increased the concentration of expression (P <0.05). In arsenic trioxide group the expression of Bmi-1 / β-actin declined with the increased concentration, a dose-dependent (r =-0.912, P<0.05), thalidomide group Bmi-1 / β-actin with the increased concentration of no significant decline (r =-0.594, P >0.05), the combined group Bmi-1 inhibition was significantly higher than arsenic trioxide, thalidomide in a separate drug group (CDI <0.7).Conclusion Thalidomide group had no significant growth inhibition. Arsenic trioxide on MUTZ-1 cells significantly inhibited the growth and increased in the combined group significantly.