岩大戟内酯B对人乳腺癌Bcap37细胞凋亡的影响

Effect of jolkinolide B on apoptosis of breast cancer Bcap37 cells

目的:探讨岩大戟内酯B(jolkinolide B)诱导人乳腺癌Bcap37细胞凋亡及其可能机制。方法:分别应用MTT和AnnexinV-FITC/PI双染法检测jolkinolide B对Bcap37细胞的生长抑制率和细胞凋亡率;用流式细胞仪检测线粒体膜电位和细胞内游离Ca2+浓度的变化;RT-PCR检测jolkinolide B对Bcap37细胞caspase-3mRNA表达的影响。结果:jolkinolide B可显著抑制Bcap37细胞的增殖,呈剂量和时间效应关系;随jolkinolide B剂量增加,细胞凋亡率明显增加;线粒体膜电位下降,并伴有细胞内游离钙浓度增加,与对照组相比差异显著(P<0.01),同时caspase-3mRNA表达水平明显增高。结论:jolkinolide B可通过提高细胞游离Ca2+水平,激活内源性线粒体信号转导途径而诱导Bcap37细胞凋亡。

Objective：To investigate the mechanism of induction of apoptosis of breast cancer Bcap37 cells by jolkinolide B.Methods：The growth inhibition of Bcap37 cells was measured by MTT method.Apoptosis was detected by AnnexinV-FITC/PI staining.The mitochondrial membrane potential and Ca2＋ levels were measured by flow cytometry.The mRNA expression level of caspase-3 was detected by RT-PCR.Results：Jolkinolide B inhibited the growth of Bcap37 cells in a dose-and time-dependent manner.Treated with jolkinolide B,the rate of cell apoptosis was increased significantly（P0.01）.Different concentrations of jolkinolide B could markedly increase the level of Ca2＋ and decrease mitochondrial membrane potential compared with the control group（P0.01）.Conclusion：Jolkinolide B has inhibitory effect on Bcap37 cell proliferation and can induce cell apoptosis.The apoptosis induced by jolkinolide B may depend on rise of intracellular Ca2＋ level in Bcap37 cells.