Aim To investigate the effects of saggliptin on vascular endothelial cell injury induced by ox-LDL and expression of miR-590/TLR4/NF-κ B. Methods Human umbilical vein endothelial cells (HUVEC) were cultured and divided into control group, ox-LDL group, sagliptin group, sagliptin+miR-590 inhibitor group, NC mimic group, miR-590 mimic group, NC inhibitor group and miR-590 inhibitor group. The proliferation activity, the expression of miR-590/TLR4/NF-κB and the contents of tumor necrosis factor-α(TNF-α), interleukin-1β (IL-1β), intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in culture medium were measured. Results The expression of TLR4, NF-κB p65 in cells and the contents of TNF-α, IL-1β, ICAM-1, VCAM-1 in culture media of ox-LDL group were significantly higher than those of control group, cell proliferation activity and the expression of miR-590 in cells was significantly lower than that of control group; the expression of TLR4, NF-κB p65 in cells and the contents of TNF-α, IL-1β, ICAM-1, VCAM-1 in culture media of sagliptin group were significantly lower than those of ox-LDL group, cell proliferation activity and the expression of miR-590 was significantly higher than that of ox-LDL group; the expression of TLR4, NF-κB p65 in cells and the contents of TNF-α, IL-1β, ICAM-1, VCAM-1 in culture media of saglitine+miR-590 inhibitor group were significantly higher than those in saglitine group, cell proliferation activity and the expression of miR-590 was significantly lower than that of saglitine group; the expression of TLR4, NF-κB p65 in cells and the contents of TNF-α, IL-1β, ICAM-1, VCAM-1 in culture media of miR-590 mimic group were significantly higher than those of NC mimic group, the expression of TLR4, NF-κB p65 in cells and the contents of TNF-α, IL-1β, ICAM-1, VCAM-1 in culture media of miR-590 inhibitor group were significantly lower than those of NC inhibitor group. Conclusion Sagliptin can alleviate ox-LDL-induced vascular endothelial cell injury by the miR-590/TLR4/NF-κB pathway.