Inhibition of NF-kappa B activity enhanced apoptosis induced by matrine in hepatocellular carcinoma cells / 中华肝脏病杂志
Chinese Journal of Hepatology
;
(12): 914-917, 2007.
Artículo
en Chino
| WPRIM
| ID: wpr-277642
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the relationship between activation of nuclear factor-kappa gene binding (NF-kappaB) and apoptosis induced by matrine in hepatocellular carcinoma cell line HepG2.</p><p><b>METHODS</b>HepG2 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).</p><p><b>RESULTS</b>PDTC 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.</p><p><b>CONCLUSIONS</b>Matrine 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.</p>
Texto completo:
Disponible
Índice:
WPRIM (Pacífico Occidental)
Asunto principal:
Patología
/
Farmacología
/
Quinolizinas
/
Tiocarbamatos
/
Prolina
/
FN-kappa B
/
Apoptosis
/
Carcinoma Hepatocelular
/
Sinergismo Farmacológico
/
Alcaloides
Límite:
Humanos
Idioma:
Chino
Revista:
Chinese Journal of Hepatology
Año:
2007
Tipo del documento:
Artículo
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