[Effect of Curcumin on the Proliferation, Apoptosis, and Cell Cycle of Human Acute Myeloid Leukemia Cell Line K562].

Ying-Ying Li, Hong-Chun Liu, Qing Zhang, Rui-Ting Feng, Yin-Sen Song, Liang Ming
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Abstract

Objective: To investigate the effects of curcumin on the proliferation, apoptosis, and cell cycle of human acute myeloid leukemia cell line K562.

Methods: MTT method was used to detect the proliferation inhibition of logarithmic growth phase human acute myeloid leukemia K562 cells, flow cytometry was used to detect the cell cycle, Annexin V-FITC was used to detect the apoptosis rate, and real-time fluorescent quantitative PCR and Western blot were used to detect the expression of Bax, BCL-2 and caspase-3 mRNA and protein, respectively.

Results: The inhibition rate of cell proliferation in curcumin 10, 20, and 40 μmol/L group for 24 h and 48 h were higher than that in the control group (curcumin 0 μmol/L), and the cell proliferation inhibition rate was concentration-time dependent (r=0.879, r=0.914). The proportion of G0/G1 cells and apoptosis rate of K562 cells in the curcumin 10, 20, and 40 μmol/L group were higher than those in the control group, and showed drug concentration dependent (r=0.856, r=0.782). The expression of Bax and Caspase-3 mRNA in the curcumin 10, 20, and 40 μmol/L group was higher, while BCL-2 mRNA was lower than those in the control group, and showed drug concentration dependent (r=0.861, r=0.748, r=-0.817). The gray value of Bax protein expression in the curcumin 10, 20, and 40 μmol/L group was higher than that in the control group, while the gray value of BCL-2 and Caspase-3 protein expression was lower than that in the control group, and showed drug concentration dependent (r=0.764, r=-0.723, r=-0.831).

Conclusion: Curcumin can inhibit the proliferation of human acute myeloid leukemia cell line K562 cells, block the cell cycle at G0/G1 phase, promote cell apoptosis, and induce apoptosis by regulating Bax, BCL-2, and Caspase-3.

姜黄素对人急性髓系白血病K562细胞增殖、凋亡和细胞周期的影响[j]。
目的:探讨姜黄素对人急性髓系白血病K562细胞增殖、凋亡及细胞周期的影响。方法:采用MTT法检测对数生长期人急性髓系白血病K562细胞的增殖抑制作用,流式细胞术检测细胞周期,Annexin V-FITC检测细胞凋亡率,实时荧光定量PCR和Western blot分别检测Bax、BCL-2和caspase-3 mRNA和蛋白的表达。结果:姜黄素10、20、40 μmol/L组对细胞增殖的抑制率均高于对照组(姜黄素0 μmol/L),且细胞增殖抑制率呈浓度-时间依赖性(r=0.879, r=0.914)。姜黄素10、20、40 μmol/L组小鼠G0/G1细胞比例和K562细胞凋亡率均高于对照组,且呈药物浓度依赖性(r=0.856, r=0.782)。姜黄素10、20、40 μmol/L组Bax、Caspase-3 mRNA表达量高于对照组,BCL-2 mRNA表达量低于对照组,且呈药物浓度依赖性(r=0.861, r=0.748, r=-0.817)。姜黄素10、20和40 μmol/L组Bax蛋白表达灰色值高于对照组,BCL-2和Caspase-3蛋白表达灰色值低于对照组,且呈药物浓度依赖性(r=0.764, r=-0.723, r=-0.831)。结论:姜黄素可抑制人急性髓系白血病K562细胞的增殖,阻断G0/G1期细胞周期,促进细胞凋亡,并通过调节Bax、BCL-2和Caspase-3诱导细胞凋亡。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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