Hyperglycemia impairs NO bioavailability and increases reactiveoxygen species (ROS) production, thereby inducing endothelial injuryand apoptosis.9,23 In the present study, we observedthat the exposure of HUVCEs to HG increased vascular permeability(Figure 6C), promotedthe transcription of ICAM1, VCAM1, and E-selectin (Figure 4A–C), and elevated theproduction of secretions of IL-8, IL-6, and IL-1β (Figure 5A–C). This evidence concerns the gene IL1B and Hyperglycemia.