Fig. 6.

Blocking NF-kB pathway rescues EDC-mediated metabolic stress and endocrine dysfunction. NF-kBi treatment decreases EDC-mediated increases in phosphorylated p65, p50, and p52 in a iFGEs and b iHTNs, *p < 0.05, **p < 0.01, ***p < 0.001. Two different cell lines were loaded in 6 lanes with lanes 1, 2, and 3 belonging to 80iCTR (Vh1, Comb1, and NF-κBi1) and lanes 4, 5, and 6 from 201iCTR (Vh2, Comb2, and NF-κBi2). c Immunocytochemistry showing phosphorylated p65 staining in vehicle treatment (Vh), increased phospho-p65 with EDC combination treatment (Comb) that decreases with NF-κBi, *p < 0.05, **p < 0.01, ***p < 0.001. d Seahorse assay showing improved mitochondrial respiration upon NF-κBi treatment compared with combination treatment in iHTNs, ***p < 0.001. e RT-qPCR expression levels of SCO2, POLRMT, TFAM, and CYB5A showing decreased mitochondrial respiratory genes with combination treatment that are rescued by NF-κBi treatment, *p < 0.05, **p < 0.01, ***p < 0.001. f Restoration of ATP levels upon NF-κBi treatment, **p < 0.01, ***p < 0.001. g α-MSH secretion levels showed improvement upon NF-κBi treatment, ***p < 0.001. h Western blot showing rescue of PYY levels in iFGEs, *p < 0.05, **p < 0.01. All statistical analysis performed using one-way ANOVA. Images and data shown are representative of average results from the two iPSC lines differentiated n = 3 times in independent experiments. Scale bars represent 50 µm. Error bars denote s.e.m