mPGES-1抑制剂MK886对白血病HL-60细胞的增殖抑制作用  

Effect of MK886,a mPGES-1 inhibitor,on proliferation in leukemia HL-60 cells

作　　者：李益清[1] 尹松梅[1] 王秀菊[1] 谢双锋[1] 聂大年[1] 马丽萍[1] 吴裕丹[1] 

机构地区：[1]中山大学孙逸仙纪念医院血液内科,广东广州510120

出　　处：《现代肿瘤医学》2013年第2期249-252,共4页Journal of Modern Oncology

基　　金：教育部高等学校博士学科点专项科研基金项目(编号:20110171120111);中央高校基本科研业务费专项资金;中山大学青年教师培育计划项目(编号:11ykpy25)

摘　　要：目的:观察膜结合型前列腺素E2合酶1(mPGES-1)抑制剂MK886对急性髓细胞白血病细胞株HL-60的增殖抑制作用。方法:不同浓度的MK886作用于HL-60细胞不同时间后,CCK-8测定其对HL-60细胞的增殖抑制率,流式细胞术检测HL-60细胞的凋亡情况,Western blot法检测mPGES-1、Bax、Bcl-2蛋白的表达,ELISA法检测PGE2。结果:HL-60细胞株高表达mPGES-1。MK886可时间、剂量依赖性地抑制HL-60细胞mPGES-1表达和PGE2合成,同时细胞增殖受到抑制,凋亡增加,Bax蛋白表达上调,Bcl-2表达下降。结论:MK886可抑制HL-60细胞增殖,诱导凋亡,其机制与下调mPGES-1表达、抑制PGE2合成和调控Bcl-2/Bax等有关。Objective ： To investigate the effects of MK886, an inhibitor of microsomal prostaglandin E synthase - 1 （ mPGES - 1 ）, on the proliferation of leukemia cell line HL - 60. Methods： HL - 60 cells were treated in vitro with MK886 by different concentration. The inhibition rates of cell growth were assayed by CCK -8 method. Cell apoptosis was analyzed by flow cytometry（FCM）. The expression of mPGES - 1, Bax and Bel -2 was detected by Western blot. PGE2 was measured by ELISA. Results： mPGES - 1 was over - expressed in human acute myeloid leukemia HL - 60cells. MK886 inhibited proliferation of HL -60 cells and induced apoptosis in a dose - and time - dependent man- ner,which may result from down- regulation of mPGES - 1 expression and PGE2 synthesis. Evaluation of mediators of apoptotic signaling revealed up - regulation of Bax expression, as well as significant decreased in Bel - 2. Conclusion：MK886 inhibited proliferation and induced apoptosis of HL -60 ceils by reducing mPGES - 1 expression and PGE2 synthesis and regulating Bcl -2/Bax expression.

关 键 词：MPGES-1 MK886 白血病 HL-60细胞 细胞增殖 

分 类 号：R73-36[医药卫生—肿瘤] R733.7[医药卫生—临床医学]