Fig. 3

CXCL5 impaired vascular endothelial function via the ERK/p65 signaling pathway in HAECs. The network formation and migration abilities were impaired after administration of CXCL5 for 2 days (n = 3; A, B). Western blotting and statistical analyses of p-ERK, p-p65, IL-1β, IL-6, and TNF-α after administration of CXCL5 for 2 days (n = 3; C, D). Western blotting and statistical analyses of VEGF and SDF-1 after administration of CXCL5 for 2 days (n = 3; E). Western blotting of CXCR2 and CXCL5 after anti-goat IgG and CXCR2 immunoprecipitation (n = 3; F). CXCL5 Chemokine C-X-C motif ligand 5, CXCR2 Chemokine C-X-C motif receptor 2, ERK extracellular signal-regulated kinase, HAEC human aortic endothelial cell, IL interleukin, SDF-1 stromal cell-derived factor 1, TNF-α tumor necrosis factor-α, VEGF vascular endothelial growth factor. N represents the number of independent experiments on different days and in different experimental runs. The Mann–Whitney U test was used to determine statistically significant differences. *p < 0.05, **p < 0.01