Objective：To investigate the effects and mechanisms of liver X receptors（LXRs） agonist T0901317 on human umbilical vein endothelial cells（HUVECs） injury induced by anoxia/reoxygenation（A/R）. Methods：HUVECs were cultivated and divided into 6 groups randomly：normal control group，anoxia（AN）group，A/R group，A/R groups with different concentrations of T0901317（0.1，１，１０ μmol/L；A/R+T 0.1 group，A/R+T 1 group，A/R+T 10 group）. The apoptosis rate of HUVECs was detected by flow cytometry. The gene expressions of intercellular adhesion molecule-1（ICAM-1） and interleukin-6（IL-6） were assessed by RT-PCR. The activ－ity of nuclear factor-κB（NF-κB） was detected by electrophoretic mobility shift assay（EMSA）. Results：Compared with those in nor－mal control group，apoptosis rates of HUVECs were increased significantly，gene expressions of inflammatory factors ICAM-1 and IL-6 were increased，activity of NF-κB was increased significantly in AN group and A/R group（P<0.05）. Compared with those in A/R group，cell apoptosis rates were decreased in A/R+T 0.1 group and A/R+T 1 group（P<0.05），gene expressions of ICAM-1 and IL-6 were inhibited in A/R+T 0.1 group and A/R+T 1 group（P<0.05），moreover，activity of NF-κB was decreased significantly in A/R+T 0.1 group and A/R+T 1 group（P<0.05）. Compared with those in A/R+T 0.1 group，cell apoptosis rates，gene expressions of ICAM-1 and IL-6 and activity of NF-κB were reduced significantly in A/R+T 1 group（P<0.05）. Conclusions：Proper dose of T0901317（0.1，1 μmol/L） can activate LXRs and protect HUVECs from A/R injury. The mechanisms of T0901317 may associate with the inhibition of NF-κB activation and downregulation of ICAM-1 and IL-6 gene expression.