HDL3 protects vascular endothelial cells from lipopolysaccharide- induced injure by inhibiting the NF-κB-mediated inflammatory reaction

[Purpose] To investigate the effects and potential mechanisms of preconditioning of high-density lipoprotein (HDL3) on lipopolysaccharide (LPS)-induced injure to human umbilical vein endothelial cells (HUVEC). [Methods] HUVECs were pretreated with HDL3 at the concentration of 50 or 100 or 200mg/L for 18 hours, washed and stimulated with LPS (1.0 mg/L) for additional 6 hours. Cell viability was measured by MTT assay. Annexin V/PI double staining was used to measure the cell apoptotic rate by flow cytometry. The numbers of THP-1 adhesion to HUVECs were observed under fluorescence microscope and the content of VCAM-1 in culture medium was measured by ELISA. The level of NF-κB p65 in cell nuclei was determined by Western blotting. [Results] LPS reduced cell viability and induced apoptosis in HUVECs. The cytotoxic effects of LPS were significantly inhibited by HDL3 pretreatment. In addition, HDL3 also significantly suppressed the LPS-induced adhesion of THP-1 to HUVECs. Meanwhile, exposure of HUVECs to LPS resulted in a significant increase in the levels of VCAM-1 in culture media and NF-κB p65 in cell nuclei. HDL3 blocked these effects in a concentration-dependent manner. [Conclusion] HDL3 can protect HUVECs from LPS-induced injure and the mechanism at least partially involves its ability to suppress the secretion of VCAM-1 and the activation of NF-κB.