Conclusion
The changed function of cholesterol efflux and some genes expression may be the pathogenetic cause, and LXR activity of macrophage may offer potential therapeutic benefit in the treatment of atherosclerosis. Thus nicotine can regulate foam cell formation by inhibiting LXR pathway.
Methods
Human monocyte-derived macrophages were collected. Before apoA-I-mediated human monocyte-derived macrophage cholesterol efflux, and mRNA expression of LXRα, and some of its target genes being detected, the macrophages were induced with or without nicotine.
Objective
This study aims to investigate the characteristics of liver X receptor α (LXRα) and its target gene expression, as well as cholesterol efflux in human macrophages treated by nicotine.
Results
Pre-incubation of Human monocyte-derived macrophages with nicotine, cholesterol efflux was suppressed to apolipoprotein AI. Nicotine also inhibited LXRα and some of its target genes mRNA expression involved cholesterol metabolism, and facilitated some inflammatory genes expression.