Isobavachalcone attenuates TNF-α-induced ICAM-1 and VCAM-1 expression in human umbilical vein endothelial cells by regulating the NF-κB signaling pathway

Abstract Vascular inflammation activated by pro-inflammatory cytokines is an inflammatory response that occurs in the early stages of atherosclerosis. Endothelial dysfunction vascular begins with expression cell surface adhesion molecules cytokines. The purpose this study was to evaluate and verify effects isobavachalcone. In study, we investigated isobavachalcone on responses induced tumor necrosis factor-α (TNF-α) human umbilical vein endothelial cells (HUVECs). TNF-α stimulation significantly increased intercellular molecule 1 (ICAM-1) (VCAM-1) proteins, concentration-dependently decreased HUVECs. Isobavachalcone suppressed TNF-α-induced ICAM-1 VCAM-1 HUVECs, thereby inhibiting increase monocyte adhesion. addition, phosphorylation NF-κB (necrosis factor κB) p65 subunit. findings demonstrate prevents has potential protect against progression