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桑根酮C通过激活caspase3及caspase9诱导前列腺癌PC3细胞凋亡

周萍 董晓先 汤平

南方医科大学学报2017,Vol.37Issue(9):1206-1210,5.
南方医科大学学报2017,Vol.37Issue(9):1206-1210,5.DOI:10.3969/j.issn.1673-4254.2017.09.11

桑根酮C通过激活caspase3及caspase9诱导前列腺癌PC3细胞凋亡

Sanggenon C induces apoptosis of prostate cancer PC3 cells by activating caspase 3 and caspase 9 pathways

周萍 1董晓先 2汤平3

作者信息

  • 1. 广州医科大学基础医学研究中心,广东广州511436
  • 2. 广州医科大学病理生理学教研室,广东广州511436
  • 3. 广州市第一人民医院泌尿外科,广东广州510180
  • 折叠

摘要

Abstract

Objective To investigate the effects of Sanggenon C in inducing apoptosis of prostate cancer PC3 cell line and explore the underlying mechanism.Methods The proliferation of PC3 cells treated for 24 h with 1,5,20,50,and 100 μmol/L sanggenon C or treated with 20 μmol/L Sanggenon C for 0,6,12,24 and 48 h was evaluated using MFT assay.Flow cytometry was performed for analysis of apoptosis of PC3 cells after exposure to sanggenon C with different treatment protocols,and the activity of caspase 3 was detected using spectrofluorometry.The inhibitory effect of sanggenon C on PC3 cells pretreated with DMSO,z-DEVD-fmk,z-LEHD-fmk or z-IETD-fmk for 1 h was detected by MTT assay.Results Sanggenon C inhibited the proliferation of PC3 cells in a dose-and time-dependent manner (P<0.05 except for 1 μrnol/L group) with a 24-h IC50 of 18.76 μmol/L.Sanggenon C at 20 μmol/L caused inhibition rates of PC3 ceils of 10.57%,27.09%,51.88%,80.73% and 87.99% after treatment for 6,12,24,48,and 72 h,respectively (P<0.05),and resulted in apoptosis rates of 7.43%,20.91% and 37.56% at 12 h,24 h and 48 h,respectively.Sanggenon C significantly increased caspase-3 activity in the cells,and its effect on PC3 cell proliferation was partially reversed by caspase 3 and caspase 9 inhibitors.Conclusion Sanggenon C can dose-dependently induce growth inhibition and apoptosis of PC3 cells possibly by activating caspase 9 and caspase 3 pathways.

关键词

桑根酮C/前列腺癌/PC3细胞/caspase/凋亡

Key words

sanggenon C/prostate cancer/PC3 cells/caspases/apoptosis

引用本文复制引用

周萍,董晓先,汤平..桑根酮C通过激活caspase3及caspase9诱导前列腺癌PC3细胞凋亡[J].南方医科大学学报,2017,37(9):1206-1210,5.

基金项目

国家自然科学基金(81072091/H1619)Supported by National Natural Science Foundation of China(81072091/H1619). (81072091/H1619)

南方医科大学学报

OA北大核心CSCDCSTPCDMEDLINE

1673-4254

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