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作 者:汪宏梅[1] 张云宁[1] 石培民[2] 谢静[2]
机构地区:[1]江苏省泰兴市人民医院检验科,江苏泰兴225400 [2]江苏省泰兴市人民医院血液科,江苏泰兴225400
出 处:《实用临床医药杂志》2013年第21期62-65,共4页Journal of Clinical Medicine in Practice
摘 要:目的观察紫杉醇体外抑制人白血病细胞SHI-1细胞的增殖活性及诱导细胞分化和凋亡的作用,并探讨其凋亡机制。方法以不同质量浓度(5、0.5、0.05、0.005 mg/L)的紫杉醇与SHI-1细胞在体外共同培养,分别作用0、12、24、36、48 h,通过细胞计数、台盼蓝染色、细胞形态学、DNA含量测定、AnnexinV/PI、细胞线粒体跨膜电位(Δφm)等分析细胞的凋亡。结果紫杉醇能促进SHI-1细胞的凋亡;0.05 mg/L紫杉醇处理对SHI-1细胞株增殖抑制及诱导凋亡作用最为显著。结论紫杉醇能抑制SHI-1细胞增殖活性,诱导细胞分化,促进细胞凋亡,使SHI-1细胞停留在G2/M期。Objective To observe the efficiency of paclitaxel in inhibiting the proliferation of human leukemia cell SHI-1 ceils and in the induction of cell differentiation, and further discuss the mechanism of apoptosis. Methods SHI-1 cells in different concentrations were cultured in vitro with paclitaxel at 0, 12h, 24h, 36h, 48 h respectively. Cellular apoptosis was then analyzed by counting cells, trypan blue staining, cell morphology, DNA content determination, Annexinv/PI and mitochon- drial transmembrane potential (Aq^m). Results Paclitaxel facilitated the cellular apoptosis, and the concentration of 0.05 mg/L was most effective in inhibiting paclitaxel SHI-1 cellular proliferation and inducing cellular apoptosis. Conclusion Paclitaxel can inhibit the proliferation of SHI-1 cells, induce its differentiation and facilitate cellular apoptosis, making SHI-1 cells stop at the stage of G2/M.
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