摘要
目的:探讨姜黄素抑制HL—60细胞增殖的机理.方法:选用HL—60细胞系,采用细胞培养,NBT还原率测定,SABC法测定BrdU摄取率,流式细胞仪检测细胞内DNA含量和原位末端TdT酶标技术,结果:姜黄素以时间、剂量依赖方式抑制HL—60细胞的增殖.在25umol/L浓度处理HL—60细胞48h,细胞增殖抑制率达60.71±1.20%,进一步分析BrdU摄取率、DNA含量分布图和NBT还原率时发现姜黄素优先使细胞阻滞于G_2/M期,随后使细胞阻滞于G_1期,整个细胞周期进程减缓,DNA合成活动受抑,阻滞细胞随之发生凋亡,而并非走向分化 同时将姜黄素对细胞周期的调控作用与VP—16、As_2O-3的结果进行比较,姜黄素调控HL—60细胞周期的能力强于As_2O_3,其作用点与VP—16也不尽完全相同,因而不存在着与后二者交叉耐药的可能性.结论:姜黄素具有一定程度调节HL—60细胞G_2/M期转换和G_1/S期转换检测点的能力,通过干扰HL—60细胞的细胞周期,诱发细胞凋亡.
Objective: To explore the active mechanisms of curcumin inhibiting HL - 60 cells proliferation. Methods:Acute myeloid leukemic cell line HL - 60 was studied by using cell culture, NBT reduction, FCM measuring DNA contents, TUNEL method determining apoptotic cell percentage. Results: Curcumin inhibited proliferation of HL - 60 cells in a dose - and time - dependent manner. When cells were treated with 25umol/ L curcumin for 48h,the inhibitory rate was 60.71±1 .20% . By analysing BrdU incoporation and the distrbu-tion of DNA content and NBT reduction, the data indicated that curcumin arrested cells in G2/M phase of cell cycle at first,then arrested cells in G0/G1 phase,the whole cell cycle progression was slow and DNA synthesis activities was halted, and the arrested cells went to apoptosis instead of differenciation. At the same time, the baility of regulating of cell cycle was stronger in curcumin group than in As2O3 group,the acting points of curcumin were not completely consistent with those of Vp-16.Thus, we guessed that the possibility of mutual resistant drug did not exist and Curcumin was able to regulate, to some extent, the G1/S and G2/M transmit checkpoint and disturbed the HL - 60 cell cycle.
出处
《现代临床医学生物工程学杂志》
CAS
1999年第3期177-179,共3页
Journal of Modern Clinical Medical Bioengineering
基金
国家自然科学基金(39770934)
