Our study showed that the expressions of eNOS and its phosphorylated form were significantly suppressed in the regenerated tissue surrounding gastric ulcer of diabetic rats (S3 Fig), which is supported by the general concept that chronic hyperglycemia impairs endothelium-derived NO biosynthesis by increased expression of caveolin-1, overproduction of reactive oxygen species (ROS), and eNOS uncoupling [31]. Here, NOS3 is linked to gastric ulcer.