Aim To explore the effect of lysophosphatidylcholine on cholesterol efflux from macrophage foam cells, and the function of calcium signaling pathway on this effect. Methods Macrophage foam cells were harvested from female mice weighing 25～30 g. Human LDL was separated from healthy subjects and isolated by differential ultracentrifugation. LDL was acytylated to ac-LDL to convert macrophage to foam cells. Cholesterol mass of medium and cells were quantified by enzymetic fluorometry. Intracellular calcium concentration was measured by fluorometry. Involvement of intracellular calcium and PKC on effect of cholesterol efflux from macrophages by LPC was measured by applying EGTA and H 7 to adduct extracellular calcium and to inhibit the activity of PKC, then observed whether cholesterol efflux could occur. Results Within the dosage of 10～80 μmol/L, LPC obviously promoted cholesterol efflux from macrophage foam cells, and LPC increased intracellular calcium concentration. When extracellular calcium was cleared by EGTA or PKC activity was inhibited by H 7, LPC could not promote cholesterol efflux from macrophage foam cells. Conclusions LPC could promote cholesterol efflux from macrophage foam cells within the dosage of 10～80 μmol/L, this effect is related to influx of intracellular calcium. Calcium-PKC signaling pathway induced LPC's effect on cholesterol efflux from macrophage foam cells.