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.
出处
《现代肿瘤医学》
CAS
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)
