[Palmitate induced apoptosis in MC3T3-E1 cell by activation of nuclear factor-kappa B].

OBJECTIVE: To explore whether palmitate-induced apoptosis of osteoblastic MC3T3-E1 cell is mediated by an activation of nuclear factor-kappa B (NF-κB). METHODS: Cell viability was assessed with methyl thiazolyl tetrazolium (MTT) assay and cell apoptosis by Hochest 33258 staining. Palmitate was added at different timepoints and dosages.Western blot was used to evaluate the expression levels of IκBα, p-NF-κB p65 and NF-κB p65 protein. RESULTS: Palmitate led to a dose- and time-dependent decreases in cell viability and increase in cell apoptosis. Cell viability dropped to 54% and cleaved caspase-3 increased 3.1-fold in cells treated with 500 µmol/L palmitate compared to control. The level of p-NF-κB p65 protein markedly increased at 60 min post-stimulation and reached a 2.96-fold increase of baseline level at 120 min (P < 0.05) . The IκBα level markedly declined at 60 min post-stimulation and decreased by 57% at 120 min (P < 0.05) . Compared to the group with palmitate treatment alone, pyrrolidine dithiocarbamic acid (10/20 µmol/L) significantly inhibited the palmitate-induced increase of p-NF-κB p65 (1.39 ± 0.12, 1.25 ± 0.10 vs 1.76 ± 0.14, both P < 0.05) , restored the palmitate-induced decrease of caspase-3 (2.24 ± 0.28 vs 1.29 ± 0.27, P < 0.05) and inhibited the palmitate-induced increase of cleaved caspase-3 (0.63 ± 0.01 vs 1.13 ± 0.10, P < 0.05) . CONCLUSION: Palmitate induces apoptosis of MC3T3-E1 cell by an activation of NF-κB.