The Effects And Mechanism Of Lxrs Agonist T0901317on Human Umbilical Vein Endothelial Cells Injury Induced By Ischemia Reperfusion

Objective:To investigate the effects and mechanism of LXRs AgonistT0901317on human umbilical vein endothelial cells (HUVECs) injury thatinduced by ischemia/reperfusion(I/R).Methods:HUVECs were cultivated and divided into6groups rand-omly:control group(CT),anoxia group(AN),I/R group(I/R),I/R+T09013170.1μmol/L group(I/R+T0.1),I/R+T09013171μmol/L group(I/R+T1), I/R+T090131710μmol/L group(I/R+T10).The apoptosis rate of HUVECs was detected by fluorescence flow cytometry.The gene expression of ICAM-1and IL-6were assessed by RT-PCR.The activation of NF-κB in the cells wasdetected by EMSA.Results: Compared with the control group,the apoptosis rate of HUV-ECs increased significantly in anoxia group and I/R group(P<0.05),the gene expression of inflammatory factors ICAM-1and IL-6increased in anoxiagroup and I/R group(P<0.05),the activation of NF-κB increased significant ly in anoxia group and I/R group（P<0.05). And compared with I/R group,the cells apoptosis rate decreased significantly in I/R+T0.1group andI/R+T1group （P<0.05),the gene expression of ICAM-1and IL-6wereinhibited in I/R+T0.1group and I/R+T1group（P<0.05),moreover, the acti-vation of NF-κB decreased significantly in I/R+T0.1group and I/R+T1group（P<0.05).Compared with I/R group, the cells apoptosis rate,the geneexpression of ICAM-1and IL-6and the activition of NF-κB in I/R+T10group had no significant difference(P>0.05).Conclusions: The ischemia/reperfusion can induce the damage ofHUVECs.Proper dose of T0901317treatment can activate Liver X receptorand inhibit the cells apoptosis rate,the gene expression of ICAM-1and IL-6,which can protect HUVECs from ischemiI/reperfusion injury. The mecha-nisms of T0901317may associate with the inhibition of NF-κ B activationand downregulation of ICAM-1and IL-6gene expression, which wouldprovide a new method for the therapy of I/R injury.