Foam cells are formed when macrophages imbibe low-density lipoprotein (LDL) through scavenger receptors. Here we examined how epigallocatechin-3-gallate (EGCG) influences foam cell formation. We found that EGCG dose-dependently reduced oxidized LDL (oxLDL) uptake in THP-1 (10 μM, 20.0 ± 0.50, p < 0.05) and primary macrophages (134.6 ± 15.6, p < 0.05) and reduced intracellular cholesterol content in these cells, respectively (10 μM, 32.6 ± 0.14, p < 0.05; 31.7 ± 1.26, p < 0.05). EGCG treatment decreased scavenger receptor A expression, but not the expression of CD36 or of reverse cholesterol transporters. Moreover, EGCG stimulated translocation of the p50 and p65 subunits of NF-κB and enhanced NF-κB DNA-binding activity, thus suppressing SR-A promoter activity. EGCG's suppression of SR-A expression was blocked by the NF-κB inhibitor Bay. The present findings suggest that EGCG regulates NF-κB activity and thus suppresses SR-A expression, oxLDL uptake, and foam cell formation.
Keywords: atherosclerosis; epigallocatechin-3-gallate; foam cells; macrophage; oxidized low-density lipoprotein.