Inhibitory Effect of Platycodin D on Proliferation of SGC7901 Cells and Moleclar Mechanism
10.16466/j.issn1005-5509.2017.07.005
- VernacularTitle:桔梗皂甙D对人胃癌细胞SGC7901增殖的抑制作用和机制研究
- Author:
Qun DAI
;
Xuan HUANG
;
Zhe CHEN
- Keywords:
PD;
SGC7901 cell apoptosis;
mitochondrial membrane potential;
bcl-2 family protein;
MAPK signal pathway
- From:
Journal of Zhejiang Chinese Medical University
2017;41(7):573-579
- CountryChina
- Language:Chinese
-
Abstract:
[Objective] To investigate the effects of platycodin D(PD) on the proliferation and apoptosis of human stomach cancer SGC7901 and the related mechanism.[Methods] SGC7901 was cultured in virto and was treated with 5～20μm·L-1 concentrations of PD.Cell proliferation was examined by MTT assay.Cell apoptosis was detected by Annexin V FITC/PI double staining.The change of mitochondrial trans-membrane potential was measured by JC-1 staining.The potein expression of cleaved caspase-3,cleaved caspase-9,cleaved PARP,bcl-2,bax,p-ERK,ERK,p-JNK,JNK,p-p38 and p38 detected by Western blot.[Results] MTT results showed that PD inhibited the growth of SGC7901 cells in a dose-dependent manner at 24h and 48h.SGC7901 cells treated with PD for 24h showed significantly enhanced apoptosis and weakened mitochondrial membrane potential compared with the control cells.Western blot results showed that PD could up-regulate expression of cleaved PARP,cleaved caspase-3,cleaved caspase-9,bax,p-JNK,p-p38 protein,decreased bcl-2,p-ERK protein,the expression of ERK,JNK,p38 protein did not change significantly.[Conclusion] PD may inhibit the proliferation and induce the apoptosis of SGC7901 cells.These findings indicated that PD inhibited cell proliferation by inhibiting the ERK signaling.PD effect on bax and bcl-2 by activation of JNK and p38 signaling pathway resulted in the decrease of mitochondrial membrane potential and activation of caspase,which induced the apoptosis of cancer cells.
