LAUSR

HighlightsLunasin ameliorated adhesion of THP‐1 monocytes to HUVECs.Lunasin suppressed the expression of VCAM‐1 and E‐selectin, but not ICAM‐1.Lunasin stimulated the expression of KLF2 mediated by the MEK5/ERK5 pathway. ABSTRACT The adherence of monocytes to endothelial cells plays a causal role in the early development of atherosclerosis and is driven by several inflammatory stimuli, which includes oxidized low‐density lipoprotein (ox‐LDL). Lunasin, a natural peptide identified in soybean seeds, soy‐derived food products, other grains and herbal plants, has been found to exert numerous biological activities, including anti‐inflammatory and antioxidant properties. However, little is known regarding the mechanism of action of lunasin in ox‐LDL‐induced endothelial inflammation. The results of the present study indicate that lunasin significantly ameliorated ox‐LDL‐induced adhesion of THP‐1 monocytes to the surface of human umbilical vein endothelial cells (HUVECs). Lunasin also suppressed expression of the adhesion molecules VCAM‐1 and E‐selectin, but not ICAM‐1. Notably, the inhibitory mechanism of lunasin is associated with its stimulatory effects on expression of the KLF2 transcriptional factor. In addition, lunasin treatment could reverse the effects of ox‐LDL on the expression of eNOS and PAI‐1, the direct target genes of KLF2. Mechanistically, it was proven that the MEK5/ERK5 pathway mediates the effects of lunasin on KLF2 expression. Taken together, the results of this study suggest that dietary or supplementary intake of lunasin may have a prophylactic or therapeutic capacity in cardiovascular diseases such as atherosclerosis.