Genistein inhibits the development of atherosclerosis via inhibiting NF-κB and VCAM-1 expression in LDLR knockout mice

Abstract

Diet can be an important factor that influences risks for cardiovascular disease. Genistein (4′,5,7-trihydroxyisoflavone), rich in soy, is one candidate that may benefit the cardiovascular system. Here, we explored the effect of genistein in atherosclerosis (AS) development in an in vivo mouse model. Low-density lipoprotein receptor (LDLR) knockout mice were allocated to control, model, and genistein groups. Our results showed that genistein significantly reduced the formation and development of atherosclerotic plaques ((4.68 ± 1.18) ×106 versus (6.65 ± 1.51) ×106 µm2, p < 0.05). In the genistein group, compared with the model group, total antioxidant capacity (TAC) level was 85.5 ± 15.6 versus 203.4 ± 32.6 mmol/L (p < 0.01); malondialdehyde (MDA) level was 3.79 ± 0.28 versus 3.06 ± 0.31 mmol/L (p < 0.01), and superoxide dismutase (SOD) activity was 86.1 ± 6.1 versus 139.1 ± 25.1 U/mL (p < 0.01). Therefore, genistein was able to enhance serum antioxidative ability in our mouse model. Genistein had no influence, however, on serum cholesterol and lipid profiles. Genistein also markedly downregulated the expression of nuclear factor (NF)-κB and vascular cell adhesion molecule (VCAM)-1 in aortas of mice (p < 0.05). These observations suggest that genistein may inhibit AS in LDLR−/− mice via enhancing serum antioxidation and downregulating NF-κB and VCAM-1 expression in the aorta.