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[Objectives] To study anti breast cancer effect and action mechanism of Dracorhodin Perchlorate( DP). [Methods] MMT was applied to analyze inhibition rate of 60 μmol / L DP to cancer cells. Cell morphological analysis,cell nucleus morphological analysis,and DNA fragment analysis were carried out to determine occurrence of cell apoptosis. Rhodamine 123 staining was conducted to analyze mitochondrial membrane potential( MMP). Western blot was used to detect cell apoptosis correlation,especially expression of mitochondria related protein.[Results]60 μmol/L DP inhibited MCF-7 growth in time-dependent manner; DP inhibited MCF-7 growth through inducing MCF-7 apoptosis;when DP induced MCF-7 apoptosis,it activated mitochondrial pathway protein caspase-9,and PARP( poly ADP ribosepolymerase) expression was decreased after DP treatment. Further study indicated that major reason for DP inducing apoptosis is that it reduced MMP( in control group,93. 11% cells kept normal MMP,but in DP-treated group,only 37. 45% cells kept normal MMP). Mitochondrial Bcl-2 and Bcl-XL were decreased,and Bax and Bak increased,which led to drop of MMP. [Conclusions] DP induced apoptosis of human breast cancer cell MCF-7 through the mitochondrial pathway.
[Objectives] To study anti breast cancer effect and action mechanism of Dracorhodin Perchlorate (DP). [Methods] MMT was applied to analyze inhibition rate of 60 μmol / L DP to cancer cells. Cell morphological analysis, cell nucleus morphological analysis, and DNA fragment analysis were carried out to determine occurrence of cell apoptosis. Rhodamine 123 staining was conducted to analyze mitochondrial membrane potential (MMP). Western blot was used to detect cell apoptosis correlation, especially expression of mitochondria related protein. [Results] 60 μmol / L DP inhibited MCF-7 growth in a time-dependent manner; DP inhibited MCF-7 growth through inducing MCF-7 apoptosis; when DP induced MCF-7 apoptosis, it activated mitochondrial pathway protein caspase-9, and PARP (poly ADP ribose polymerase) expression was decreased after DP treatment. Further study indicated that major reason for DP inducing apoptosis is that it reduced MMP (in control group, 93. 11% cells kept normal MMP, but in DP-treated grove up, only 37. 45% cells kept normal MMP). Mitochondrial Bcl-2 and Bcl-XL were decreased, and Bax and Bak increased, which led to drop of MMP. [Conclusions] DP induced apoptosis of human breast cancer cell MCF- 7 through the mitochondrial pathway.