Inhibitory Effects of Periplocin from Cortex Periplocae on Human Lung Cancer Cell Line QG56
10.3969/j.issn.0253-9896.2014.03.002
- VernacularTitle:香加皮杠柳苷对人肺癌QG56细胞抑制作用的研究
- Author:
Jing ZHANG
;
Guang YANG
;
Xuetao ZHAO
;
Baoen SHAN
;
Jianghui LIU
- Publication Type:Journal Article
- Keywords:
lung neoplasms;
Cortex Periplocae;
Periploca Sepium;
cell proliferation;
cell cycle;
apoptosis;
proto-on-cogene proteins c-bcl-2;
periplocin from cortex periplocae;
bax
- From:
Tianjin Medical Journal
2014;(3):197-199
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the inhibitory effects of periplocin from cortex periplocae (CPP) on human lung cancer cell line QG56 and to discuss its mechanism. Methods QG56 cells were cultured in vitro. The final concentrations of CPP in control group were 1.25, 2.50, 5.00, 10.00 and 20.00μg/L. QG56 cells were treated with ascending concentration of CPP for 24 h, 48 h and 72 h. The cell proliferation was measured using MTT method. The morphological changes of QG56 cells were observed under inverted microscope. Flow cytometry (FCM) was used to detect the effects of CPP on cell cycle and cell apoptosis. The expression of apoptosis associated gene bax mRNA in QG56 cells was detected by RT-PCR. The expres-sion of bax protein before and after treatment of CPP was examined by SP immunocytochemistry. Results The inhibitory ef-fect of CPP on the proliferation of QG56 cells was increased with the increasing concentrations of CPP and the prolonged du-ration of treatment. The morphological changes were displayed in QG56 exposed to CPP. The results of FCM showed that CPP caused cell cycle arrest at G0/G1 phase. The apoptotic rate of QG56 cells was significantly increased after CPP treatment for 48 h (P<0.05). The expression of bax mRNA was increased in QG56 exposed to CPP. The result of immunocytochemis-try indicated that CPP up-regulated the expression of bax protein. Conclusion CPP showed significant inhibitory effect on human lung cancer cell lines QG56 through inducing cell cycle arrest and apoptosis.
