Inhibition of NF-kappa B activity enhanced apoptosis induced by matrine in hepatocellular carcinoma cells.
- Author:
Hang GAO
1
;
Song HE
;
Wei-Xue TANG
;
Jue WANG
Author Information
- Publication Type:Journal Article
- MeSH: Alkaloids; pharmacology; Apoptosis; drug effects; Carcinoma, Hepatocellular; pathology; Drug Synergism; Hep G2 Cells; Humans; Liver Neoplasms; pathology; NF-kappa B; metabolism; Proline; analogs & derivatives; pharmacology; Quinolizines; pharmacology; Thiocarbamates; pharmacology
- From: Chinese Journal of Hepatology 2007;15(12):914-917
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the relationship between activation of nuclear factor-kappa gene binding (NF-kappaB) and apoptosis induced by matrine in hepatocellular carcinoma cell line HepG2.
METHODSHepG2 cells were stimulated by different concentrations of matrine (0.8, 1.0, 1.5, 2.0, 2.5 g/L). The HepG2 cell survival rates were evaluated by MTT assay. Cultured HepG2 cells were implanted in culture flasks and divided into four groups: a control group, a pyrrolidine dithiocarbamate (PDTC) group (20 micromol/L), a matrine group (1.5 g/L) and a combination group, PDTC (20 micromol/L) + matrine (1.5 g/L) combination group. Apoptosis induced by matrine was analyzed by flow cytometry (FCM) and TUNEL. The DNA-binding activity of NF-kappaB was determined by electrophoretic mobility shift assay (EMSA).
RESULTSPDTC enhanced the inhibition of matrine on cell proliferation (F=183.92, P less than 0.01). The apoptosis and activation of NF-kappaB of HepG2 cells were induced by matrine. PDTC significantly suppressed NF-kappaB activation induced by matrine in HepG2 cells. PDTC increased the apoptosis induced by matrine of the HepG2 cells from 6.11% +/- 0.81% to 12.95% +/- 0.02%, chi2=9.67, P less than 0.01.
CONCLUSIONSMatrine could induce apoptosis, and at the same time induce activation of NF-kappaB in HepG2 cells. PDTC increases the apoptosis in hepatocellular carcinoma cells and it may be related to suppressing NF-kB activation of HepG2 cells.