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桑根酮C通过激活半胱天冬酶3和半胱天冬酶9通路诱导前列腺癌PC3细胞凋亡

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

作者信息

Zhou Ping, Dong Xiao-Xian, Tang Ping

机构信息

Basic Medical Research Center, Guangzhou Medical University, Guangzhou 511436, China.E-mail:

出版信息

Nan Fang Yi Ke Da Xue Xue Bao. 2017 Sep 20;37(9):1206-1210. doi: 10.3969/j.issn.1673-4254.2017.09.11.

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 MTT 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 µmol/L group) with a 24-h IC of 18.76 µmol/L. Sanggenon C at 20 µmol/L caused inhibition rates of PC3 cells 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.

摘要

目的

研究桑根酮C诱导前列腺癌PC3细胞系凋亡的作用,并探讨其潜在机制。

方法

采用MTT法评估用1、5、20、50和100 μmol/L桑根酮C处理24小时的PC3细胞,或用20 μmol/L桑根酮C处理0、6、12、24和48小时的PC3细胞的增殖情况。采用流式细胞术分析不同处理方案的桑根酮C作用后PC3细胞的凋亡情况,并用荧光分光光度法检测caspase 3的活性。通过MTT法检测桑根酮C对用二甲基亚砜(DMSO)、z-DEVD-fmk、z-LEHD-fmk或z-IETD-fmk预处理1小时的PC3细胞的抑制作用。

结果

桑根酮C以剂量和时间依赖性方式抑制PC3细胞的增殖(除1 μmol/L组外,P<0.05),24小时半数抑制浓度(IC)为18.76 μmol/L。20 μmol/L桑根酮C处理6、12、24、48和72小时后,PC3细胞的抑制率分别为10.57%、27.09%、51.88%、80.73%和87.99%(P<0.05),在12小时、24小时和48小时的凋亡率分别为7.43%、20.91%和37.56%。桑根酮C显著增加细胞中caspase-3的活性,caspase 3和caspase 9抑制剂可部分逆转其对PC3细胞增殖的影响。

结论

桑根酮C可能通过激活caspase 9和caspase 3途径,剂量依赖性地诱导PC3细胞生长抑制和凋亡。

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