Pachymic Acid Inhibits OX-LDL-induced Injury In Human Umbilical Vein Endothelial Cells Via Activating Nrf2/HO-1 Signaling Pathway

Objective: To study the effect of Pachymic acid(PA)on oxidative stress injury of human umbilical vein endothelial cells induced by oxidized low-density lipoprotein(OX-LDL)and its signaling pathway.Methods: Human umbilical vein endothelial cells(HUVEC)were pretreated with different concentrations of PA for 12 h,and then OX-LDL was added to stimulate HUVEC for 24 h.Cell viability of HUVEC and apoptotic rate were detected by CCK-8 and Annexin V-FITC/PI staining respectively.SOD activity and MDA content in the cells were detected by commercial kits.Intracellular reactive oxygen species(ROS)was detected by Chemical fluorescence method.The expression of apoptosis-related proteins(Bcl2,Bax,Caspase-3)and pathway protein Nrf2 /HO-1 were detected by Western blot.The mRNA expression of Nrf2 /HO-1 in the endothelial cells were detected by RT-PCR.Results: OX-LDL treatment significantly reduced the cell activity ofHUVEC,triggered the cell apoptosis,increased the content of pro-oxidant(MDA)and intracellular ROS,upregulated the expression of Caspase-3,Bax and decreased the activity of antioxidant(SOD)and the expression of Bcl-2,Nrf2 and HO-1.Interestingly,these changes induced by OX-LDL were reversed by the pretreatment of PA.The protective effect of PA could be eliminated by zinc protoporphyrin(a specific inhibitor of HO-1).Conclusion: Pachymic acid(PA)can improve HUVEC cell viability interfered by OX-LDL,reduce the apoptosis of cells and the oxidative stress injury,which may be related to the activation of Nrf2 /HO-1signaling pathway.