The Effect of Ginsenoside Rg3 on Breast Cancer MCF-7 Mitochondrial Pathway of Apoptosis

Objective To study the mitochondrial apoptotic pathway induced by 20 (R)- ginsenoside Rg3 (SPG-Rg3) in human breast cancer MCF-7 cells and the mechanism of induction of apoptosis. Methods Human breast cancer cell line MCF-7 cells were divided into control group,experimental control group and SPG-Rg3 multiple concentrations. MTT was adopted to observe the restraining growth effect intervented by ginsenoside Rg3,and the half inhibitory concentration(IC-50) was calculated to further determine the effective concentration;Flow cytometry was adopted to detect MCF-7 cell cycle after the role of Ginsenoside Rg3;Annexin V- EGFP/PI double staining was adopted to detect of Ginsenoside Rg3 induced apoptosis of MCF-7 cells;Immunocytochemistry was used to detect the relationship between MCF-7 cell apoptosis and expression of cytochrome C protein. Results 20(R)-ginsenoside Rg3 on the growth of MCF-7 breast cancer cells significantly inhibited,and the inhibition rate increased with the increase of its concentration. 20(R) -ginsenoside Rg3 on MCF-7 breast cancer cells in IC-50 in 48h,respectively 244.54μg/mL;Flow cytometry results showed that: 300μg/mL 20(R)-the role of ginsenoside Rg3 in MCF-7 cells 48 hours after S phase cells increased significantly(P0.01),G2-M phase cells decreased significantly (P 0.05),MCF-7 cell apoptosis was significantly increased (P 0.01);Cytochrome C protein immunocytochemistry showed that:In experimental groups,levels of cytosolic cytochrome C were significantly higher (P 0.01). Conclusion SPG-Rg3 on MCF-7 breast cancer cells significantly inhibited;SPG-Rg3 can induce apoptosis in MCF-7 breast cancer. The occurrence mechanism of death may be induced by cytochrome C released from mitochondrial.