The Anti-Atherosclerotic Effect of Naringin Is Associated with Reduced Expressions of Cell Adhesion Molecules and Chemokines through NF-κB Pathway

Naringin has been reported to have an anti-atherosclerosis effect but the underlying mechanism is not fully understood. The aim of this study is to investigate the impact of naringin on the TNF--induced expressions of cell adhesion molecules, chemokines and NF-B signaling pathway in human umbilical vein endothelial cells (HUVECs). The experiments revealed that naringin, at concentrations without cytotoxicity, dose-dependently inhibited the adhesion of THP-1 monocytes to the TNF--stimulated HUVECs. The TNF--induced expressions of cell adhesion molecules, including VCAM-1, ICAM-1 and E-selectin, at both the mRNA and protein levels, were significantly suppressed by naringin in a dose dependent manner. In addition, the TNF--induced mRNA and protein levels of chemokines, including fractalkine/CX3CL1, MCP-1 and RANTES, were also reduced by naringin. Naringin significantly inhibited TNF--induced nuclear translocation of NF-B, which resulted from the inhibited phosphorylation of IKK/, IB- and NF-B. Altogether, we proposed that naringin modulated TNF--induced expressions of cell adhesion molecules and chemokines through the inhibition of TNF--induced activation of IKK/NF-B signaling pathway to exert the anti-atherosclerotic effect.