Type 2 diabetes mellitus (T2DM) is associated with chronic low‑grade inflammation. Carvacrol has been confirmed to possess anti‑inflammatory properties, but its effect on diabetic vasculature remains unknown. The aim of the present study was to investigate the possible protective effects of carvacrol against vascular endothelial inflammation. The mice were divided into four groups (n=15 per group) as follows: Non‑diabetic control mice, db/db mice, db/db mice + carvacrol (low) and db/db mice + carvacrol (high) groups. The effects of carvacrol on the pathomorphism of the thoracoabdominal aorta in db/db mice were evaluated using hematoxylin and eosin and Masson's trichrome staining. The serum levels of insulin signaling molecules, such as phosphorylated insulin receptor, phosphorylated insulin receptor substrate‑1, insulin, triglyceride (TG) and inflammatory cytokines [tumor necrosis factor‑α, interleukin (IL)‑1β, IL‑6 and IL‑8] were measured by ELISA. Furthermore, the protein levels of the toll‑like receptor (TLR)4/nuclear factor (NF)‑κB inflammatory signaling pathway molecules were investigated in the thoracoabdominal aorta of db/db mice and in high glucose‑induced endothelial cells. Vascular endothelial cell apoptosis and viability were assessed by using flow cytometry and Cell Counting Kit‑8 assays, respectively. The results demonstrated that carvacrol alleviated vascular endothelial cell injury. Carvacrol reduced the expression levels of insulin signaling molecules, insulin, TG and inflammatory cytokines in the serum of db/db mice. Moreover, carvacrol reduced the activation of the TLR4/NF‑κB signaling pathway in vivo and in vitro. In vitro, carvacrol inhibited high glucose‑induced endothelial cell function by promoting vascular endothelial cell apoptosis and suppressing cell viability. These findings demonstrated that carvacrol could alleviate endothelial dysfunction and vascular inflammation in T2DM.