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机构地区:[1]中国科学院上海细胞生物学研究所,上海200031
出 处:《实验生物学报》2000年第1期13-20,共8页Acta Biologiae Experimentalis Sinica
基 金:国家自然科学基金(NO.39893320);上海市科技启明星计划资助项目~~
摘 要:本文应用流式细胞分选仪和电子显微镜研究了IL-3和羟基脲对人红白血病细胞株(K562细胞)凋亡的影响。结果显示:IL-3和羟基脲分别诱导K562细胞,不能引起细胞凋亡;而IL-3和羟基脲协同诱导K562细胞,可以引起细胞凋亡。用流式细胞仪检测到IL-3和羟基脲协同诱导K562细胞后,DNA含量低于二倍体的细胞数达31.90%,并产生明显的凋亡小峰。同时,IL-3和羟基脲协同诱导K562细胞, 可抑制细胞周期中的S期,阻止细胞从S期进入G_2/M期,使细胞周期延长,对K562细胞的生长和增殖具有抑制作用。在电镜下可观察到IL-3和羟基脲协同诱导的K562细胞,出现典型的凋亡细胞形态,细胞核内染色质浓缩、凝聚,紧靠在核膜边沿,形成新月形或环状的染色质结构,产生凋亡小体。提示:IL-3和羟基脲具有协同效应,IL-3可提高K562细胞对羟基脲的敏感性,并可协同羟基脲诱导K562细胞凋亡。The effect of IL-3 and hydroxyurea on human erythroleukemia cell line (K562 cells) was demonstrated by using the electro-microscopy and flow cytometry. Our data showed that neither IL-3 nor hydroxyurea could induce the apop-tosis of K562 cells alone. However, the IL-3 and hydroxyurea could induce the apoptosis of K562 cells cooperatively. Analysis with flow cytometry showed that the percentage of apoptotic cells was about 31. 90% after K562 cells were induced by IL-3 and hydroxyurea cooperatively for 5 days, and the sub-G, peak (apoptotic peak) was detect- ed in the induced K562 cells. Meanwhile, the percentage of S-phase in the IL-3 and hydroxyurea induced K562 cells was increased, and the proliferation of the induced K562 cells was inhibited significantly. Furthermore, the IL-3 and hydroxyurea induced K562 cells showed chromatin condensation with regular crescents at the nuclear edges and apoptotic bodies. It suggested that IL-3 could enhance the sensitivity of K562 cells to hydroxyurea and the apoptosis of K562 cells could be induced by IL-3 and hydroxyurea cooperatively.
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