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자료유형
학술저널
저자정보
Zhang, Hong (Department of Pharmacology, School of Pharmaceutical Sciences, Jilin University) Xu, Hua-Li (Department of Pharmacology, School of Pharmaceutical Sciences, Jilin University) Fu, Wen-Wen (Department of Pharmacology, School of Pharmaceutical Sciences, Jilin University) Xin, Ying (Department of Pharmacology, School of Pharmaceutical Sciences, Jilin University) Li, Mao-Wei (Department of Pharmacology, School of Pharmaceutical Sciences, Jilin University) Wang, Shuai-Jun (Department of Pharmacology, School of Pharmaceutical Sciences, Jilin University) Yu, Xiao-Feng (Department of Pharmacology, School of Pharmaceutical Sciences, Jilin University) Sui, Da-Yun (Department of Pharmacology, School of Pharmaceutical Sciences, Jilin University)
저널정보
아시아태평양암예방학회 Asian Pacific journal of cancer prevention : APJCP Asian Pacific journal of cancer prevention : APJCP 제15권 제18호
발행연도
2014.1
수록면
7,919 - 7,923 (5page)

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20(S)-Protopanaxadiol (PPD), a ginsenoside isolated from Pananx quinquefolium L., has been shown to inhibit growth and proliferation in several cancer cell lines. The aim of this study was to evaluate its anticancer activity in human breast cancer cells. MCF-7 cells were incubated with different concentrations of 20(S)-PPD and cytotoxicity was evaluated by MTT assay. Occurrence of apoptosis was detected by DAPI and Annexin V-FITC/PI double staining. Mitochondrial membrane potential was measured with Rhodamine 123. The Bcl-2 and Bax expression were determined by Western blot analysis. Caspase activity was measured by colorimetric assay. 20(S)-PPD dose-dependently inhibited cell proliferation in MCF-7 cells, with an $IC_{50}$ value of $33.3{\mu}M$ at 24h. MCF-7 cells treated with 20(S)-PPD presented typical apoptosis, as observed by morphological analysis in cell stained with DAPI. The percentages of annexin V-FITC positive cells were 8.92%, 17.8%, 24.5% and 30.5% in MCF-7 cells treated with 0, 15, 30 and $60{\mu}M$ of 20(S)-PPD, respectively. Moreover, 20(S)-PPD could induce mitochondrial membrane potential loss, up-regulate Bax expression and down-regulate Bcl-2 expression. These events paralleled activation of caspase-9, -3 and PARP cleavage. Apoptosis induced by 20(S)-PPD was blocked by z-VAD-fmk, a pan-caspase inhibitor, suggesting induction of caspase-mediated apoptotic cell death. In conclusion, the 20(S)-PPD investigated is able to inhibit cell proliferation and to induce cancer cell death by a caspase-mediated apoptosis pathway.

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