Fig. 3

Silencing of SAA1 exerts an inhibitory effect over PA-induced insulin resistance via the activation of the NF-κB pathway. a, the gray value of cytoplasmic p65 and nucleus p65 protein bands according to the western blot analysis; b, the protein expression of cytoplasmic p65 and nucleus p65 in response to the treatment of PA + sh-SAA1, PA + pcDNA3, PA + pcDNA3-SAA1; *, p < 0.05 vs. the blank group; #, p < 0.05 vs. the PA + sh-NC group; &, p < 0.05 vs. the PA + pcDNA3 group; c, the mRNA expression of IRS1 and SOCS3 in response to the treatment of PA + BAY, PA + sh-SAA1 + BAY, PA + pcDNA3-SAA1 + BAY determined by RT-qPCR; *, p < 0.05 vs. the PA group; #, p < 0.05 vs. the PA + BAY group; d, the gray value of IRS1, p-IRS1 and SOCS3 protein bands in response to the treatment of PA + BAY, PA + sh-SAA1 + BAY, PA + pcDNA3-SAA1 + BAY according to the western blot analysis; e, the protein expression of IRS1 and SOCS3, and the extent of IRS1 phosphorylation in response to the treatment of PA + BAY, PA + sh-SAA1 + BAY, PA + pcDNA3-SAA1 + BAY according to western blot analysis; *, p < 0.05 vs. the PA group; #, p < 0.05 vs. the PA + BAY group; f, 2DG uptake in response to the treatment of insulin + PA + BAY, insulin + PA + sh-SAA1 + BAY, insulin + PA + pcDNA3-SAA1 + BAY; p < 0.05 vs. the insulin + PA group; #, p < 0.05 vs. the insulin + PA + BAY group; data were expressed by means ± standard deviation; multiple groups were compared by one-way analysis of variance; the experiment was repeated 3 times; SAA1, serum amyloid A protein 1; NF-κB, nuclear factor-κB; 2DG, [3H]2-Deoxyglucose Uptake; PA, palmitate; RT-qPCR, reverse transcription quantitative polymerase chain reaction; SOCS3, suppressor of cytokine signaling 3; IRS1, insulin receptor substrate 1; p-IRS1, phosphorylated IRS1; NC, negative control