Aim Toinvestigatetheinducementeffect of isatin on apoptosis of breast cancer cell line MCF-7 , andexploreitsdetailedmechanism.Methods MCF-7 cell lines were exposed to isatin at different concentra-tions(0,50,100,200 μmol·L-1 )for 48 h.Apop-totic features were demonstrated by nuclei staining with Hoechst 33258.Bcl-2,Bax and p53 mRNA were ana-lyzed by RT-PCR.Caspase-9 activation and mitochon-drial depolarization were assayed by flow cytometry. Bcl-2,Bax,p53 and cytochrome c proteins were ana-lyzedbyWesternblot.Results Isatininducesapopto-sis of MCF-7 cells.Furthermore,Bcl-2 expression was decreased and the ratio of Bcl-2 to Bax was significant-ly decreased by isatin.While,p53 expression relative-ly decreased.The mitochondrial transmembrane poten-tial was markedly reduced and the release of cyto-chrome c into the cytosol was increased after treatment with isatin.Simultaneously,caspase-9 was activated. Conclusions Isatinsignificantlyinducedtheapopto-sis of MCF-7 cells in vitro.These results strongly sug-gest that the p53 dependent mitochondrial pathway is involved in apoptosis.%目的探讨吲哚醌（isatin）对乳腺癌细胞MCF-7的抗肿瘤作用及其具体的调控机制。方法不同浓度isatin（0、50、100、200μmol·L－1）作用于乳腺癌细胞48 h后，利用细胞荧光染色、RT-PCR、Western blot及流式细胞术等方法检测isatin的促凋亡作用。结果不同浓度isatin处理MCF-7细胞48 h，荧光显微镜观察到细胞出现核染色质聚集、细胞体积缩小及DNA断裂等典型的凋亡形态学改变。RT-PCR和Western blot结果证实，随着isatin浓度的不断增加，p53、Bax mRNA和蛋白表达量也逐渐增加，而Bcl-2 mRNA及蛋白表达下降；流式细胞仪结果提示不同药物浓度作用的细胞膜电位出现不同程度的下降，caspase-9被激活。Western blot结果显示isatin处理组细胞胞质细胞色素C含量明显增加，相反线粒体中细胞色素C含量相应降低。结论 isatin具有明显诱导乳腺癌细胞MCF-7凋亡的作用，其可能的作用机制是经p53的线粒体凋亡通路被激活。
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