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作 者:李莹莹[1] 刘红春[2] 张倾 冯睿婷 宋银森 明亮[2] LI Ying-Ying;LIU Hong-Chun;ZHANG Qing;FENG Rui-Ting;SONG Yin-Sen;MING Liang(Translational Medicine Research Center,People's Hospital of Zhengzhou,Zhengzhou 450o00,Henan Province,China;Department of Clinical Laboratory,The First Affiliated Hospital of Zhengzhou University,Zhengzhou 450002,Henan Province,China)
机构地区:[1]郑州人民医院转化医学研究中心,河南郑州450000 [2]郑州大学第一附属医院检验科,河南郑州450002
出 处:《中国实验血液学杂志》2022年第5期1343-1347,共5页Journal of Experimental Hematology
摘 要:目的:探讨姜黄素对人急性髓系白血病细胞株K562增殖、凋亡及细胞周期的影响。方法:取对数生长期人急性髓系白血病K562细胞,用MTT法测定细胞增殖抑制情况,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法和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和40μmol/L组培养24 h和48 h细胞增殖抑制率均高于对照组(姜黄素0μmol/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和40μmol/L组G_(0)/G_(1)细胞比例和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和40μmol/L组Bax和Caspase-3 mRNA表达高于对照组,而BCL-2 mRNA表达低于对照组,且呈药物浓度依赖性(r=0.861,r=0.748,r=-0.817)。姜黄素10、20和40μmol/L组Bax蛋白表达灰度值高于对照组,而BCL-2和Caspase-3蛋白表达灰度值低于对照组,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细胞株K562细胞增殖,将细胞周期阻滞于G_(0)/G_(1)期,促进细胞凋亡,且通过调控Bax、BCL-2和Caspase-3而诱导K562细胞凋亡。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 G/Gcells 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 G_(0)/G_(1) phase, promote cell apoptosis, and induce apoptosis by regulating Bax, BCL-2, and Caspase-3.
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