The anti-proliferation effect of gypenosides on cervical cancer HeLa cells and its molecular mechanism
10.3781/j.issn.1000-7431.2013.10.004
- Author:
Miao GAO
1
Author Information
1. Department of Nursing
- Publication Type:Journal Article
- Keywords:
Apoptosis;
Cell proliferation;
Gypenoside;
HeLa cells;
Uterine cervical neoplasms
- From:
Tumor
2013;33(10):868-872
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To investigate the inhibitory effect of gypenosides on proliferation of human uterine cervical cancer HeLa cells in vitro, and to explore its possible mechanism. Methods: The HeLa cells were treated with different concentrations of gypenosides (low-dose group, 4.5 μg/mL; middle-dose group, 45 μg/mL; high-dose group, 450 μg/mL). The cells treated with 0.9% sodium chloride solution was designed as a control group. The inhibitory effect of gypenosides on the proliferation of HeLa cells was detected by MTT assay and BrdU (5-bromo-2-deoxyuridine) incorporation experiment. The effect of gypenosides on apoptosis of HeLa cells was detected by FCM (flow cytometry). The expression levels of Bcl-2, Bax, ERK1/2 (extracellular regulated protein kinase 1/2), p-ERK1/2 (phospho-ERK1/2), MEK1/2 (mitogen-activated protein kinase kinase) and p-MEK1/2 were detected by Western blotting. Results: The survival rate of HeLa cells was decreased significantly after treatment with gypenosides (45 μg/mL) at 24 h (P < 0.01). The survival rate of HeLa cells was decreased significantly after treatment with gypenosides (4.5 μg/mL) at 48 h (P < 0.01). The inhibitory effect of gypenosides (450 μg/mL) on the cell proliferation was confirmed by BrdU incorporation experiment. The apoptotic rate of HeLa cells was increased significantly after treatment with different concentrations of gypenosides. Gypenosides could down-regulate the expression levels of Bcl-2 and p-ERK1/2 and up-regulate the expression level of Bax. Conclusion: Gypenosides can significantly inhibit the proliferation of cervical cancer HeLa cells and also markedly induce the apoptosis. This effect may related to the up-regulation of Bax expression and down-regulation of Bcl-2 and p-ERK1/2 expressions. Copyright © 2013 by TUMOR.
