Fig. 6

Liver kinase B1 (LKB1) is essential for liraglutide-stimulated NO production in HUVECs. HUVECs were serum-starved with EBM-2 (0.1% FBS and growth factor-free) for 6 h, and proteins were extracted after stimulation with liraglutide (10 nmol/L) for the indicated time; a representative western blot images of phosphorylated (p-) and total (t-) LKB1, AMPK, and endothelial NOS (eNOS) at 0, 5, 10, and 20 min; b–d ratio of p- to t-LKB1, AMPK, and eNOS 20 min after liraglutide stimulation, n = 4–6; *p < 0.05, **p < 0.01 vs. 0 min. Predesigned siRNAs for negative control or LKB1 were transfected to HUVECs at 25 nmol/L. HUVECs were used for experiments 72 h post-transfection; e, f representative western blot images of LKB1 and β-actin 72 h after siRNA transfection, and ratio of LKB1 to β-actin, n = 4; ^†p < 0.05; g effects of LKB1 knockdown on liraglutide-stimulated NO production; h–j representative western blot images of siRNA-transfected HUVECs 20 min after liraglutide stimulation, and ratio of p- to t-AMPK and eNOS, n = 5–6; ^†p < 0.05