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[Inhibitory effect of norcantharidin combined with evodiamine on the growth of human hepatic carcinoma cell line HepG2 in vitro].

Authors :
Liu Y
Zahng J
You Z
Liao H
Source :
Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology [Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi] 2014 Aug; Vol. 30 (8), pp. 824-8.
Publication Year :
2014

Abstract

Objective: To investigate the combined effect of evodiamine (EVO) and norcantharidin (NCTD) on HepG2 cells.<br />Methods: HepG2 cells were treated with EVO or/and NCTD at different concentrations in vitro, with blank culture medium as the negative control. The inhibitory effect of EVO or/and NCTD was determined by MTT assay. Cell cycle and cell apoptosis were assessed by flow cytometry (FCM) combined with PI staining and annexin V-FITC/PI, respectively. The expressions of Bax and Bcl-2 were examined by Western blotting. RESULTS MTT assay showed that NCTD and EVO had restraining effect on the growth of HepG2 cells. The combination of NCTD and EVO had significant synergistic inhibition effect (CI<1). The arrest rate of G2/M phase was (36.13±1.63)% in the EVO induced group and (10.67±0.89)% in the NCTD induced group, and the combination of EVO and NCTD up-regulated the rate to (73.42±1.92)% (P<0.05). In addition, the apoptosis rate of HepG2 cells treated by two-drug combination increased significantly from (15.78 ± 3.08)% in the EVO group and (11.47 ± 1.60)% in the NCTD group to (21.86±2.70)% in the EVO combined with NCTD group (P<0.05). Western blotting demonstrated that the expression level of Bax protein went up significantly (P<0.05), meanwhile Bcl-2 protein dropped significantly (P<0.05) in the combined induced group.<br />Conclusion: EVO combined with NCTD showed synergetic effect on anti-proliferation and pro-apoptosis in HepG2 cells.

Details

Language :
Chinese
ISSN :
1007-8738
Volume :
30
Issue :
8
Database :
MEDLINE
Journal :
Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology
Publication Type :
Academic Journal
Accession number :
25108435