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作 者:李赛 潘磊[2] 高瑞兰[2] 赵燕娜[2] 余潇苓[2] 尹利明[2] LI Sai;PAN Lei;GAO Rui-lan;ZHAO Yan-na;YU Xiao-ling;YIN Li-ming(The First Clinical Medical College of Zhejiang Chinese Medical University, Hangzhou 310053, China;The First Affiliated Hospital of Zhejiang Chinese Medicine University, Hangzhou 310006, China)
机构地区:[1]浙江中医药大学第一临床医学院,浙江杭州310053 [2]浙江中医药大学附属第一医院,浙江杭州310006
出 处:《中国病理生理杂志》2019年第4期592-596,共5页Chinese Journal of Pathophysiology
基 金:国家自然科学基金资助项目(No.81774068);浙江省自然科学基金资助项目(No.LY16H270006; No.LY18H290004; No.LY14H280004)
摘 要:目的:探讨蛇六谷提取物(TuAKe)抑制人慢性髓系白血病K562细胞增殖和诱导分化的作用机制。方法:不同浓度的TuAKe处理K562细胞,MTT比色法和半固体集落形成实验检测K562细胞的增殖能力;瑞氏-姬姆萨染色观察细胞形态;流式细胞术检测分化相关抗原CD11b、CD14和CD42b的阳性表达率;Western blot法检测细胞周期蛋白依赖性激酶2(CDK2)、细胞周期蛋白E1(cyclin E1)和红系分化核转录因子GATA-1的蛋白表达水平。结果:TuAKe能够抑制K562细胞增殖,改变细胞形态,抑制K562细胞进入S期,并阻滞在G_2/M期,提高分化相关抗原CD11b、CD14和CD42b阳性表达率,上调GATA-1蛋白表达,同时下调CDK2和cyclin E1蛋白表达(P<0.05)。结论:TuAKe可能通过调控细胞周期抑制K562细胞增殖,同时诱导K562细胞多向分化。AIM: To investigate the effects of Sheliugu extract(the extract from Amorphophallus konjac tuber, TuAKe) on the proliferation and differentiation of human chronic myeloid leukemia K562 cells. METHODS: TuAKe at different concentrations was used to treat with the K562 cells. The colony formation ability of the cells was detected by the colony formation assay with semi-solid culture. The viability of K562 cells was measured by MTT assay. The morphological changes of the cells were observed under microscope with Wright-Giemsa staining. The positive expression rates of differentiation-related antigens CD11 b, CD14 and CD42 b were analyzed by flow cytometry. The protein expression of cyclin-dependent kinase 2(CDK2), cyclin E1 and erythroid cell differentiation nuclear transcription factor GATA-1 was determined by Western blot. RESULTS: TuAKe reduced the proliferation of K562 cells, reduced nuclear mass ratio, inhibited K562 cells to enter S phase, and blocked the cells in G2/M phase. TuAKe improved the positive expression rates of differentiation-related antigens CD11 b, CD14 and CD42 b, increased GATA-1 protein expression, and decreased the protein expression of CDK2 and cyclin E1(P<0.05). CONCLUSION: TuAKe may inhibit K562 cell proliferation by regulating cell cycle, and induce K562 cell multidirectional differentiation at the same time.
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