Fig. 5

Effects of exenatide on Th17/Treg proliferation via PI3K/Akt/FoxO1 signaling. A mRNA levels of FoxO1 in PBMCs from control (Con) and exenatide (Exe) groups detected by real-time PCR. mRNA quantities were calculated as a ratio to the level of GAPDH mRNA in each sample. Data are shown as the relative expression ratio to Con 0 Week. Results are expressed as mean ± SEM, n = 8 in each group. B Representative image and gray value analysis of Foxo1 and phosphor (p)-FoxO1 in PBMCs from Con and Exe groups detected by western blot. ACTIN was used as a loading control. Data are shown as the relative expression ratio to Con 0 Week and expressed as mean ± SEM, n = 8 in each group. C Th17 cells were treated with palmitate (PA), exenatide plus palmitate (Exe + PA) and exenatide, palmitate plus FxoO1 inhibitor AS1842856 (Exe + PA + AS). Representative image of total PI3K, Akt, FoxO1 and p-PI3K, p-Akt, p-FoxO1 in Th17 cells in vitro detected by western blot. D Gray value analysis of p-PI3K/PI3K, p-Akt/Akt and p-FoxO1/FoxO1 in Th17 cells. E Gray value analysis of p-PI3K, p-Akt and p-FoxO1 in Th17 cells. F Treg cells were treated with PA, Exe + PA and Exe + PA + AS. Representative image of total PI3K, Akt, FoxO1 and p-PI3K, p-Akt, p-FoxO1 in Treg cells in vitro detected by western blot. G Gray value analysis of p-PI3K/PI3K, p-Akt/Akt and p-FoxO1/FoxO1 in Treg cells. H Gray value analysis of p-PI3K, p-Akt and p-FoxO1 in Treg cells. Data are shown as the relative expression ratio to Control. Three independent experiments were performed and results are expressed as mean ± SEM. **P < 0.01, *P < 0.05 vs control 0 week (A, B), or control group (D, E, G, H); & P < 0.01, ^#P < 0.05 vs control 8 week (A, B), or PA group (D, E, G, H); ns P > 0.05