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目的 :探讨姜黄素对 HL- 6 0细胞周期的影响。方法 :选取 HL- 6 0细胞系 ,作细胞培养 ,采用 SABC法测定分化抗原 CD1 1 a和 CD1 4 阳性率 ,用 TU NEL 法判定细胞凋亡 ,用 FCM法分析细胞周期 ,检测 p2 7kip1、p2 1waf1、cyclin D3及 p Rb P-表达率。结果 :姜黄素呈时间及剂量依赖性抑制 HL- 6 0细胞增殖 ,用 5、10、2 5 μmol/ L 作用 18h,增殖抑制率为 4.7± 1.2 %、18.0± 2 .0 %和 37.5± 2 .4% ;2 4h后抑制率达 6 .3± 1.9%、2 5 .0± 2 .2 %和 43.8±2 .0 % ,可增加 p2 7kip1、p2 1waf1表达 ,降低 cyclin D3表达 ,使去磷酸化 p Rb(p Rb P- )表达量增高 ;用 10 μmol/ L 姜黄素作用 4d,p2 7kip1 、p2 1waf1 、p Rb P- 阳性率为 47.8± 3.6 %、42 .7± 2 .2 %和 2 3.5± 1.5 % ,FCM进一步发现姜黄素作用后 ,p2 7kip1 、cyclin D3荧光强度分别较对照组增高 7倍及降低 74.93%。细胞周期被阻滞于 G0 / G1 和 G2 / M期 ,进而走向凋亡 ,且此能力呈时间及剂量依赖性。结论 :姜黄素能干扰细胞周期进程 ,诱导 HL - 6 0细胞凋亡 ,其作用机制与上调 p2 7kip1 、p2 1waf1 及下调 Cyclin D3蛋白表达 ,增加 p Rb P- 表达水平 ,调控 G1 / S和 G2 / M期检测点功能有关。
Objective: To investigate the effect of curcumin on the cell cycle of HL-60 cells. METHODS: HL-60 cell line was selected for cell culture. The positive rate of differentiation antigen CD1 1 a and CD1 4 was determined by SABC method. Apoptosis was determined by TU NEL method. The cell cycle was analyzed by FCM method, and p2 7kip1 and p2 were detected. 1waf1, cyclin D3, and p Rb P-expression rates. RESULTS: Curcumin inhibited the proliferation of HL-60 cells in a dose-and time-dependent manner. The effects of curcumin at 5, 10, and 25 μmol / L for 18 hours were 4.7± 1.2%, 18.0± 2%, and 37.5± 2 respectively. The inhibition rate of .4%;2 after 4 hours reached 6.3±1.9%, 25.0%±2.2%, and 43.8±2.0%, which could increase the expression of p2 7kip1, p2 1waf1, and decrease the expression of cyclin D3. The expression of phosphorylated p Rb(p Rb P- ) was increased; when treated with 10 μmol/L curcumin for 4 days, the positive rates of p2 7kip1, p2 1waf1, and p Rb P- were 47.8±3.6% and 42.7±2.2%. And 2 3.5 ± 1.5%, FCM further found that the effect of curcumin, p2 7kip1, cyclin D3 fluorescence intensity than the control group increased by 7 times and decreased by 74.93%. The cell cycle is arrested in the G0/G1 and G2 / M phases, which leads to apoptosis, and this ability is time and dose dependent. CONCLUSION: Curcumin can interfere with cell cycle progression and induce apoptosis of HL-60 cells. Its mechanism of action is to up-regulate p2 7kip1, p2 1waf1 and down-regulate Cyclin D3 protein expression, increase p Rb P-expression level, regulate G1 / S and G2 / M detection point function related.