Effect of Atorvastatin on mRNA Expression of Liver X Receptor α and Its Target Gene in Human Umbilical Vein Endothelial Cells Induced by Lipopolysacharide

Aim To investigate the effect of atorvastatin on mRNA expression of liver X receptor α(LXRα) and its target gene ATP-binding cassette transporter A1(ABCA1),sterol regulatory element binding protein-1(SREBP-1) in human umbilical vein endothelial cells(HUVEC) after treated by lipopolysacharide(LPS).Methods Human umbilical vein endothelial cells were cultured in vitro with gibco 1640 medium and 10 percent fetal bovine serum and 1 percent double antibiotics,and then were plated in 6-well plates at a denisity of approximately 2×105 cells per milliliter of media to be intervened.(1)Control group: HUVEC were cultured with the completed medium involving phosphate buffered saline(PBS),and LPS treated group or control intervention group: HUVEC were treated with LPS(the terminal concentration was 100 μg/L) for 24 hours;(2)Atorvastatin intervention group or control intervention group:HUVEC were first treated with atorvastatin at different concentrations(0.1,1.0,10.0 μmol/L) or dimethyl sulfoxide(DMSO) for 2 hours,and then co-treated with LPS for 22 hours.The level of LXRα and its target genes mRNA expression were measured by real-time polymerase chain reaction.Results Compared with control group,LPS could inhibit the mRNA expression of LXRα and its target genes ABCA1,SREBP-1 in HUVEC.The differences were statistically significant(P0.05).Compared with LPS plus DMSO group,atorvastatin could upregulate the mRNA expression of LXRα and its target gene mRNA expression in a dose-dependent manner.The differences were statistically significant(P0.05).Meanwhile,atorvastatin could downregulate the mRNA expression of inflammatory factor and adhesion factors in a dose-dependent manner.Conclusion These results demonstrate that LPS may inhibit the mRNA expression of LXRα and its target genes in HUVEC,and atorvastatin can upregulate the mRNA expression of LXRα and its target gene mRNA expression in a dose-dependent manner to inhibit the inflammatory state of HUVEC.