When AP occurs, a large number of inflammatory mediators such as tumor necrosis factor-α, interleukins (e.g., interleukin-1, interleukin-6), and reactive oxygen species (ROS) are released, and these inflammatory mediators can injure endothelial cells through multiple pathways and trigger endothelial dysfunction (12, 13, 26). This evidence concerns the gene IL6 and endothelial dysfunction.