Fig. 2

UC-MSCs attenuated PA–LPS-induced inflammation and improved insulin sensitivity in vitro. HepG2 cells were treated with PA + LPS, CM, L-DMEM, UC-MSCs, and fibroblasts accordingly. (a–d) mRNA of NLRP3, IL-1β, IL-18, and TNF-α analyzed by quantitative RT-PCR. Values shown as fold change to the blank control. Protein levels were detected in HepG2 cells by ELISA for IL-1β (e), IL-18 (f), and TNF-α (g). (h) Activity of caspase-1 assayed for each group. (i, j) Glucose metabolism of HepG2 cells in different groups by glycogen assay kit or glucose assay kit. (k) Western blot analysis of NLRP3, p-IRS (Ser307), IRS, PI3K, p-AKT (Thr308), AKT, and Glut4 of each group. Ratios of NLRP3, PI3K, Glut4 to β-actin, p-IRS to IRS, and p-AKT to AKT were quantitated. *P < 0.05, **P < 0.01. IL interleukin, LPS lipopolysaccharide, PA palmitic acid, TNF tumor necrosis factor, UC-MSC umbilical cord-derived mesenchymal stem cell