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作 者:黄韧敏[1] 袁淑兰[1] 宋毅[1] 黄光琦[1]
机构地区:[1]华西医科大学肿瘤研究所
出 处:《癌症》1998年第3期164-166,I000,共4页Chinese Journal of Cancer
摘 要:目的:在以往对丹参酮IA诱导分化和抗癌作用研究的基础上,进一步研究丹参酮IA诱导HL-60细胞凋亡,以探讨其抗癌作用机理。方法:应用体外细胞培养技术,以1~10μg/ml丹参酮IA作用于培养的HL-60细胞5天后,进行光镜、电镜、琼脂糖凝胶电泳及流式细胞仪的观察和分析。结果:丹参酮ⅡA作用后,HL-60细胞的生长受到明显抑制,其半数抑制浓度IC50约为10μg/ml光镜、电镜观察到细胞呈现凋亡特征,琼脂糖凝胶电泳显示细胞DNA呈梯状降解,流式细胞仪分析表明,10μg/ml丹参酮ⅡA作用后,HL-60细胞凋亡率达28.8%,细胞被阻止于G0/G1期,S期细胞明显减少(P<0.01),其bcl-2基因的表达显著降低,而p53基因的表达增强(P<0.01)。结论:丹参酮ⅡA可诱导HL-60细胞凋亡,这可能为丹参酮ⅡA抗癌抑癌的重要机理之一,诱导分化与诱导凋亡之间的关系有待进一步探讨。Purpose: Based on the tumor cell differentiation and antitumor effects induced by Tanshinone, the apoptosis of HL-60 cells induced by Tanshinone IIA was studied in order to find out the mechanism of the antitumor effect of Tanshinone IIA. Methods: By techniques of cell culture in vitro, HL-60 cells were treated by Tanshinone IIA in 1~10 μg/ml concentrations for 5 days, then observed and analysed by light microscopy, electronic microscopy, agarose gel electrophoresis and Flow-Cytometry (FCM). Results: The growth of HL-60 cells was inhibited evidently after treatment by Tanshinone IIA, the 50% inhibitory concentration (IC50) was about 10 μg/ml. The cells showed characters of apoptosis observed by light and electronic microscopy, Agarose gel electrophoresis of DNA showd change of “ladder” pattern. The ratio of apoptosis is 28.8% when treated with 10 μg/ml Tanshinone IIA, and the cell was inhibited in G0/G1 phase, the cells in S phase decreased (P<0.01). The expression of bc1-2 gene protein decreased obviously and p53 gene protein increasd when analysed by FCM (P<0.01). Conclusions: The results once more confirmed that Tanshinone IIA could induce the apoptosis of HL-60 cells, which may be one of the important mechanisms of Tanshinone IIA's antitumor effects. Further work about the relationship between cell differentiation and apoptosis induced is needed.
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