ABSTRACT
Objective To investigate the apoptosis of HepG2 cells and their sensitivities to the ciglitazone after inhibiting the activity of nuclear factor-kappa B (NF-kB) by NF-kB decoy oligonucleotide. Methods After transfecting HepG2 cells with NF-kB decoy oligonucleotide, the activity of NF-kB was observed by electrophonetic mobility shift assay and the protein expression of Bcl-2 and Fas by Western blot. The transfected and untransfected HepG2 cells were processed with 100 umol/L of ciglitazone for 1 to 4 days, and the growth curve and cell cycle of HepG2 cells were observed. Results After transfecting NF-kB decoy oligonucleotide to HepG2 cells, the activity of the NF-kB was inhibited, the Bcl-2 protein expression decreased and the Fas protein expression increased. The inhibition effect of the ciglitazone on the growth of HepG2 ceils was strengthened and more HepG2 cells were arrested at G1/G0 phase. Conclusions NF-kB decoy oligonucleotide could accelerate the apoptosis of HepG2 cells and enhance the inhibition effect of ciglitazone on HepG2 proliferation, the mechanism of which might be attributable to the increased expression of Fas protein and the decreased expression of Bcl-2 protein after NF-kB decoy oligonucleotide inhibiting the activity of NF-kB.