详细信息
羊栖菜多糖诱导HL-60细胞凋亡的研究 被引量:26
STUDY ON THE APOPTOSIS OF HL-60 HUMAN PROMYELOID LEUKAEMIA CELLS INDUCED BY SFPS
文献类型:期刊文献
中文题名:羊栖菜多糖诱导HL-60细胞凋亡的研究
英文题名:STUDY ON THE APOPTOSIS OF HL-60 HUMAN PROMYELOID LEUKAEMIA CELLS INDUCED BY SFPS
作者:梁倩[1];李继承[1];张华芳[2]
机构:[1]浙江大学细胞生物学研究所;[2]绍兴文理学院
年份:2004
卷号:37
期号:2
起止页码:125
中文期刊名:实验生物学报
外文期刊名:Acta Biologiae Experimentalis Sinica
收录:MEDLINE(收录号:15259985)、CSTPCD、、北大核心2000、Scopus(收录号:2-s2.0-16544393521)、CSCD2011_2012、北大核心、CSCD、PubMed
基金:浙江省中医药科研基金
语种:中文
中文关键词:羊栖菜多糖;流式细胞术;HL-60细胞;肿瘤;细胞凋亡
外文关键词:Apoptosis. Sargassum fusiforme. Polysaccharides. Tumour. HL-60 cell.Flow cytometry
中文摘要:用MTT法观察羊栖菜多糖(SFPS)在体外抗人白血病HL-60细胞增殖作用;扫描电镜、透射电镜、DNA电泳和流式细胞仪检测HL-60细胞凋亡。结果表明SFPS对HL-60细胞具有显著生长抑制作用,并呈量效和时效关系,药物作用24,36,48,72h的IC_(50)分别为390,362,402,421mg/L;药物浓度为300mg/L和500mg/L作用HL-60细胞后,琼脂糖凝胶电泳显示有凋亡细胞特有的DNA梯状条带,细胞微绒毛减少、染色质固缩、过集,凋亡小体形成;DNA直方图出现亚G_1峰。在一定浓度范围内,SFPS诱导细胞凋亡的作用呈现浓度和时间依赖性,同时G_2/M期细胞比例增多。因此,SFPS抗肿瘤作用与诱导细胞凋亡和G_2/M期细胞阻滞有关。
外文摘要:The inhibition effects of Sargassum fusiforme Polysaccharides (SFPS) on proliferation of human HL-60 promyeloid leukemia cells were measured by MTT assay. SFPS-induced apoptosis in HL-60 cells was observed by electron microscopy, flow cytometry and DNA electrophoresis. The results revealed that SFPS exhibited antiproliferative activity which depended on dosage and time. After incubation for 24,36,48 and 72h, SFPS had growth inhibitory effect on HL-60 cells with IC50 of 390,362,402 and 421mg/L. A ladder-like pattern of DNA fragmentation was demonstrated on agarose gel electrophoresis after HL-60 cells induced by SFPS at a dose of 300mg/L and 500mg/ L. Morphological examination by electron microscopy showed cells with few mierovilli on the surface, chromatin condensation and margination, cell shrinkage and the presence of 'apoptosis bodies'. The DNA content analysis of FCM showed pre-G1 cells and increased G2 period ratio, in addition, it demonstrated that apoptosis induced by SFPS was dose-and time-dependent. In conclusion, the antitumor effect of SFPS is relative to cell apoptosis and the blocking of G2/M period cells.
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