白血病·淋巴瘤
白血病·淋巴瘤
백혈병·림파류
JOURNAL OF LEUKEMIA & LYMPHOMA
2012年
9期
513-516
,共4页
李益清%尹松梅%马丽萍%聂大年%谢双锋%王秀菊%吴裕丹
李益清%尹鬆梅%馬麗萍%聶大年%謝雙鋒%王秀菊%吳裕丹
리익청%윤송매%마려평%섭대년%사쌍봉%왕수국%오유단
白血病,实验性%细胞周期%MK886%膜结合型前列腺素E2合酶1
白血病,實驗性%細胞週期%MK886%膜結閤型前列腺素E2閤酶1
백혈병,실험성%세포주기%MK886%막결합형전렬선소E2합매1
Leukemia,experimental%Cell cycle%MK886%Membrane-bound prostaglandin E2 synthase 1
目的 探讨膜结合型前列腺素E2合酶1(mPGES-1)抑制剂MK886对人类急性髓系白血病耐药细胞HL-60/A细胞周期的作用.方法 采用流式细胞术、Western blot、酶联免疫吸附(ELISA)等方法,检测HL-60/A及健康人单个核细胞(MNC)、敏感细胞株HL-60的细胞周期、mPGES-1蛋白、细胞周期索D1( cyclin D1)的差异,检测不同浓度的MK886对HL-60/A细胞周期的作用及对cyclin D1、mPGES-1、PGE2、P-Akt、c-myc蛋白的影响.结果 与健康人MNC及敏感细胞株HL-60比较,HL-60/A细胞cyclin D1 、mPGES-1表达最高,G0～G1期细胞比例为(30.53±2.15)％,较正常MNC[( 62.63±6.58 )％]及HL-60细胞[(38 86±2 25)％]减少(均P＜0.05)；S期比例为(57.56±1.54)％,较正常MNC[(12 18±4.43)％]及HL-60细胞[(47.70±1.88)％]明显增多(均P＜0.05).MK886作用后,被阻滞于G0～G1期的细胞增多,同时mPGES-1表达下调,合成PGE2减少,cyclin D1、P-Akt、c-myc蛋白表达下降.结论 MK886对白血病HL-60/A细胞有细胞周期阻滞作用,其机制与抑制mPGES-1表达,减少PGE2的合成,抑制cyclin DI、P-Akt、c-myc表达有关.
目的 探討膜結閤型前列腺素E2閤酶1(mPGES-1)抑製劑MK886對人類急性髓繫白血病耐藥細胞HL-60/A細胞週期的作用.方法 採用流式細胞術、Western blot、酶聯免疫吸附(ELISA)等方法,檢測HL-60/A及健康人單箇覈細胞(MNC)、敏感細胞株HL-60的細胞週期、mPGES-1蛋白、細胞週期索D1( cyclin D1)的差異,檢測不同濃度的MK886對HL-60/A細胞週期的作用及對cyclin D1、mPGES-1、PGE2、P-Akt、c-myc蛋白的影響.結果 與健康人MNC及敏感細胞株HL-60比較,HL-60/A細胞cyclin D1 、mPGES-1錶達最高,G0～G1期細胞比例為(30.53±2.15)％,較正常MNC[( 62.63±6.58 )％]及HL-60細胞[(38 86±2 25)％]減少(均P＜0.05)；S期比例為(57.56±1.54)％,較正常MNC[(12 18±4.43)％]及HL-60細胞[(47.70±1.88)％]明顯增多(均P＜0.05).MK886作用後,被阻滯于G0～G1期的細胞增多,同時mPGES-1錶達下調,閤成PGE2減少,cyclin D1、P-Akt、c-myc蛋白錶達下降.結論 MK886對白血病HL-60/A細胞有細胞週期阻滯作用,其機製與抑製mPGES-1錶達,減少PGE2的閤成,抑製cyclin DI、P-Akt、c-myc錶達有關.
목적 탐토막결합형전렬선소E2합매1(mPGES-1)억제제MK886대인류급성수계백혈병내약세포HL-60/A세포주기적작용.방법 채용류식세포술、Western blot、매련면역흡부(ELISA)등방법,검측HL-60/A급건강인단개핵세포(MNC)、민감세포주HL-60적세포주기、mPGES-1단백、세포주기색D1( cyclin D1)적차이,검측불동농도적MK886대HL-60/A세포주기적작용급대cyclin D1、mPGES-1、PGE2、P-Akt、c-myc단백적영향.결과 여건강인MNC급민감세포주HL-60비교,HL-60/A세포cyclin D1 、mPGES-1표체최고,G0～G1기세포비례위(30.53±2.15)％,교정상MNC[( 62.63±6.58 )％]급HL-60세포[(38 86±2 25)％]감소(균P＜0.05)；S기비례위(57.56±1.54)％,교정상MNC[(12 18±4.43)％]급HL-60세포[(47.70±1.88)％]명현증다(균P＜0.05).MK886작용후,피조체우G0～G1기적세포증다,동시mPGES-1표체하조,합성PGE2감소,cyclin D1、P-Akt、c-myc단백표체하강.결론 MK886대백혈병HL-60/A세포유세포주기조체작용,기궤제여억제mPGES-1표체,감소PGE2적합성,억제cyclin DI、P-Akt、c-myc표체유관.
Objective To investigate the effect of membrane-bound prostaglandin E2 synthase 1 (mPGES-1) inhibitor MK886 on cell cycle of the human acute myeloid leukemia HL-60/A cells.Methods Flow cytometry,Western blot and ELISA were used to measure the difference of cell cycle,expression of cyclin D1, mPGES-1 among HL-60/A cells,MNC and HL-60 cells.The effect of MK886 on cell cycle,cyclin D1,mPGES-1,PGE2,P-Akt and c-myc of HL-60/A cells were observed.Results Compared with MNC and HL-60 cells,the expression of cyclin D1 and mPGES-1 were higher in HL-60/A cells,the percentage of G0-G1 phase was decreased [MNC (62.63±6.58) ％,HL-60 (38.86±2.25) ％,HL-60/A (30.53±2.15) ％]and S phase increased[MNC (12.18±4.43) ％,HL-60 (47.70±1.88）％,HL-60/A (57.56±1.54) ％](all P＜ 0.05).After treated with MK886,cell cycle was arrested in G0-G1 phase.The expression of mPGES-1,cyclin D1,P-Akt and c-myc and synthesis of PGE2 were decreased.Conclusion MK886 can arrest HL-60/A cell cycles in G0-G1 phase,which possibly through down-regulation of mPGES-1/PGE2,reduction cyclin D1,P-Akt and c-myc expression.
