Figures & data
Figure 1. Vildagliptin inhibits FFA-induced endothelial lactate dehydrogenase (LDH) release. Human umbilical vein endothelial cells (HUVECs) were treated with high FFAs (1 mM) in the presence or absence of vildagliptin (2.5, 5 μM) for 48 h. LDH release was determined using a commercial kit (a, b, c, p < .01 vs. previous column group).
![Figure 1. Vildagliptin inhibits FFA-induced endothelial lactate dehydrogenase (LDH) release. Human umbilical vein endothelial cells (HUVECs) were treated with high FFAs (1 mM) in the presence or absence of vildagliptin (2.5, 5 μM) for 48 h. LDH release was determined using a commercial kit (a, b, c, p < .01 vs. previous column group).](/cms/asset/1af78835-47ee-47c1-9ef5-b3389ef331a5/ianb_a_1578783_f0001_b.jpg)
Figure 2. Vildagliptin suppresses FFA-induced endothelial generation of reactive oxygen species (ROS) and reduction of glutathione (GSH). (A). Intracellular ROS was determined by DCFH-DA; (B). Intracellular GSH levels. Human umbilical vein endothelial cells (HUVECs) were treated with high FFAs (1 mM) in the presence or absence of vildagliptin (2.5, 5 μM) for 48 h (a, b, c, p < .01 vs. previous column group).
![Figure 2. Vildagliptin suppresses FFA-induced endothelial generation of reactive oxygen species (ROS) and reduction of glutathione (GSH). (A). Intracellular ROS was determined by DCFH-DA; (B). Intracellular GSH levels. Human umbilical vein endothelial cells (HUVECs) were treated with high FFAs (1 mM) in the presence or absence of vildagliptin (2.5, 5 μM) for 48 h (a, b, c, p < .01 vs. previous column group).](/cms/asset/6d26c16b-fedb-40b4-9b19-f3f0056e220b/ianb_a_1578783_f0002_c.jpg)
Figure 3. Vildagliptin suppresses FFA-mediated endothelial NOX-4 elevation. Human umbilical vein endothelial cells (HUVECs) were treated with high FFAs (1 mM) in the presence or absence of vildagliptin (2.5, 5 μM) for 24 h. (A). mRNA levels of NOX-4 as determined by real-time PCR; (B). Protein levels of NOX-4 determined by western blot analysis (a, b, c, p < .01 vs. previous column group).
![Figure 3. Vildagliptin suppresses FFA-mediated endothelial NOX-4 elevation. Human umbilical vein endothelial cells (HUVECs) were treated with high FFAs (1 mM) in the presence or absence of vildagliptin (2.5, 5 μM) for 24 h. (A). mRNA levels of NOX-4 as determined by real-time PCR; (B). Protein levels of NOX-4 determined by western blot analysis (a, b, c, p < .01 vs. previous column group).](/cms/asset/ce613826-b7da-416e-a473-0f3e10f88089/ianb_a_1578783_f0003_b.jpg)
Figure 4. Vildagliptin restores FFA-induced reduced endothelial mitochondrial membrane potential (MMP). Human umbilical vein endothelial cells (HUVECs) were treated with high FFAs (1 mM) in the presence or absence of vildagliptin (2.5 μM, 5 μM) for 48 h. MMP levels were determined by TMRM staining (a, b, c, p < .01 vs. previous column group).
![Figure 4. Vildagliptin restores FFA-induced reduced endothelial mitochondrial membrane potential (MMP). Human umbilical vein endothelial cells (HUVECs) were treated with high FFAs (1 mM) in the presence or absence of vildagliptin (2.5 μM, 5 μM) for 48 h. MMP levels were determined by TMRM staining (a, b, c, p < .01 vs. previous column group).](/cms/asset/d7191b83-b00a-4131-97e0-dc8e9fd37d7f/ianb_a_1578783_f0004_c.jpg)
Figure 5. Vildagliptin prevents FFA-induced endothelial NLRP3 inflammasome activation. Human umbilical vein endothelial cells (HUVECs) were treated with high FFAs (1 mM) in the presence or absence of vildagliptin (2.5, 5 μM) for 24 h. (A). Western blot analysis of NLRP3, ASC, and cleaved caspase 1 (P20); (B). Quantification of western blot results (a, b, c, p < .01 vs. previous column group).
![Figure 5. Vildagliptin prevents FFA-induced endothelial NLRP3 inflammasome activation. Human umbilical vein endothelial cells (HUVECs) were treated with high FFAs (1 mM) in the presence or absence of vildagliptin (2.5, 5 μM) for 24 h. (A). Western blot analysis of NLRP3, ASC, and cleaved caspase 1 (P20); (B). Quantification of western blot results (a, b, c, p < .01 vs. previous column group).](/cms/asset/59fc54e2-b7d3-4e2c-a2a6-f83084bd6b88/ianb_a_1578783_f0005_b.jpg)
Figure 6. Vildagliptin inhibits FFA-induced maturation of IL-1β and IL-18. (A). Secretion of IL-1β was assessed by ELISA; (B). Secretion of IL-18 was assessed by ELISA. Human umbilical vein endothelial cells (HUVECs) were treated with high FFAs (1 mM) in the presence or absence of vildagliptin (2.5, 5 μM) for 48 h (a, b, c, p < .01 vs. previous column group).
![Figure 6. Vildagliptin inhibits FFA-induced maturation of IL-1β and IL-18. (A). Secretion of IL-1β was assessed by ELISA; (B). Secretion of IL-18 was assessed by ELISA. Human umbilical vein endothelial cells (HUVECs) were treated with high FFAs (1 mM) in the presence or absence of vildagliptin (2.5, 5 μM) for 48 h (a, b, c, p < .01 vs. previous column group).](/cms/asset/1621f2a6-aad0-452c-9ccb-d3c01835e5e5/ianb_a_1578783_f0006_b.jpg)
Figure 7. Vildagliptin inhibits FFA-induced release of high mobility group box-1 protein (HMGB1). Human umbilical vein endothelial cells (HUVECs) were treated with high FFAs (1 mM) in the presence or absence of vildagliptin (2.5 μM, 5 μM) for 48 h. Secretion of HMGB1 was determined by ELISA (a, b, c, p < .01 vs. previous column group).
![Figure 7. Vildagliptin inhibits FFA-induced release of high mobility group box-1 protein (HMGB1). Human umbilical vein endothelial cells (HUVECs) were treated with high FFAs (1 mM) in the presence or absence of vildagliptin (2.5 μM, 5 μM) for 48 h. Secretion of HMGB1 was determined by ELISA (a, b, c, p < .01 vs. previous column group).](/cms/asset/7793a58d-227b-43fe-b7c1-ef38e35f15b8/ianb_a_1578783_f0007_b.jpg)
Figure 8. Vildagliptin mitigates FFA-induced AMPK inactivation. Human umbilical vein endothelial cells (HUVECs) were treated with high FFAs (1 mM) in the presence or absence of vildagliptin (2.5 μM, 5 μM) for 6 h. Phosphorylated and total AMPK was determined by western blot analysis (a, b, c, p<.01 vs. previous column group).
![Figure 8. Vildagliptin mitigates FFA-induced AMPK inactivation. Human umbilical vein endothelial cells (HUVECs) were treated with high FFAs (1 mM) in the presence or absence of vildagliptin (2.5 μM, 5 μM) for 6 h. Phosphorylated and total AMPK was determined by western blot analysis (a, b, c, p<.01 vs. previous column group).](/cms/asset/1e8129c1-db45-4ed5-bd5a-54e0551bf3bb/ianb_a_1578783_f0008_b.jpg)
Figure 9. Vildagliptin suppresses FFA-induced reduction of eNOS. Human umbilical vein endothelial cells (HUVECs) were treated with high FFAs (1 mM) in the presence or absence of vildagliptin (2.5 μM, 5 μM) for 24 h. eNOS was determined by Western blot analysis (a, b, c, p < .01 vs. previous column group).
![Figure 9. Vildagliptin suppresses FFA-induced reduction of eNOS. Human umbilical vein endothelial cells (HUVECs) were treated with high FFAs (1 mM) in the presence or absence of vildagliptin (2.5 μM, 5 μM) for 24 h. eNOS was determined by Western blot analysis (a, b, c, p < .01 vs. previous column group).](/cms/asset/5d6b2fa0-7db0-45ef-b37a-3a1433e33436/ianb_a_1578783_f0009_b.jpg)