Treatment with TUDCA to DM rats showed that acetylcholine-mediated relaxation involved the eNOS/PI3K/Akt pathway, NAD(P)H oxidase, and endothelial KATP channel, which are similar to those in control rats (Figure 7; (d) the expressions of eNOS and Akt proteins were downregulated in DM compared to control rats and upregulated after treatment with TUDCA; and (e) levels of oxidative stress markers (SOD activity and MDA level) and the pro-inflammatory marker, IL-6, were high in the aorta of DM compared to control rats. This evidence concerns the gene IL6 and diabetes mellitus.