布法林
细胞凋亡
HL60型
白血病
DNA断裂
生物
分子生物学
碎片(计算)
环己酰亚胺
化学
细胞生物学
程序性细胞死亡
生物化学
免疫学
蛋白质生物合成
生态学
作者
Yutaka Masuda,N Kawazoe,Shigeo Nakajo,Takemi Yoshida,Yukio Kuroiwa,Kazuyasu Nakaya
标识
DOI:10.1016/0145-2126(95)00031-i
摘要
A low concentration of bufalin, a component of bufadienoides in the traditional Chinese medicine chan'su, was shown previously to induce differentiation of a broad range of human leukemia cell lines. In the present study, we found that bufalin at concentrations of 10−7 M and higher induced apoptosis in human leukemia cells, such as HL60, ML1, but not in mouse leukemia M1 cells. A mere 15 min pretreatment of HL60 cells with 10−6 M bufalin, followed by incubation for 15 h without bufalin, caused fragmentation of DNA and a decrease in cell viability, indicating that the signal for induction of apoptosis is triggered rapidly upon treatment with bufalin. Bufalin-induced apoptosis in HL60 cells was inhibited by ZnCl2, an inhibitor of endonuclease, but not by cycloheximide, an inhibitor of protein synthesis. Northern blot analysis revealed that the levels of expression of the c-myc and bcl-2 genes in HL60 cells decreased with time after treatment with bufalin. These results suggest that bufalin induces apoptosis specifically in human leukemia cells by altering the expression of these genes involved in apoptosis.
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