核转录因子-kB圈套寡核苷酸对肝癌HepG2细胞凋亡的影响

Effects of nuclear factor-kappa B decoy oligonucleotide on the apoptosis of HepG2 cells

目的观察核转录因子-kB（nuclearfactor—kappaB，NF—kB）圈套寡核苷酸抑制NF—kB活性后，肝癌HepG2细胞凋亡情况及其对环格列酮敏感性的变化。方法将NF—kB圈套寡核苷酸转染肝癌HepG2细胞，检测NF—kB活性以及凋亡相关蛋白Bcl-2和Fas的变化。以100μmol／L的环格列酮处理转染和未转染的细胞1～4d，观察肝癌HepG2细胞的生长曲线和细胞周期分布情况。结果转染后的肝癌HepG2细胞NF—kB活性明显下降，Bcl-2表达减少和Fas表达增加，并且环格列酮抑制肝癌HepG2细胞增殖的作用增强，更多的细胞被阻滞于G1／G0期。结论NF—kB圈套寡核苷酸可促进肝癌HepG2细胞的凋亡，增加肝癌HepG2细胞对环格列酮的敏感性，可能与NF—kB圈套寡核苷酸通过下调NF—kB的活性使凋亡蛋白Fas表达增加和凋亡抑制蛋白Bcl-2表达减少有关。

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 oligonueleotide. Methods After transfeeting HepG2 cells with NF-kB decoy oligonueleotide, the activity of NF-kB was observed by electrophonetie mobility shift assay and the protein expression of Bel-2 and Fas by Western blot. The transfeeted and untransfeeted HepG2 cells were processed with 100 μmol/L of eiglitazone for 1 to 4 days, and the growth curve and cell cycle of HepG2 cells were observed. Results After transfeeting NF-kB decoy oligonueleotide to HepG2 cells, the activity of the NF-kB was inhibited, the Bel-2 protein expression decreased and the Fas protein expression increased. The inhibition effect of the eiglitazone on the growth of HepG2 cells was strengthened and more HepG2 cells were arrested at G1/G0 phase. Conclusions NF-kB decoy oligonueleotide 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 Bel-2 protein after NF-kB decoy oligonueleotide inhibiting the activity of NF-kB.