Cynandione A inhibits lipopolysaccharide-induced cell adhesion via suppression of the protein expression of VCAM‑1 in human endothelial cells.

Cynandione A (CA) is one of the most active compounds in the roots of Cynanchum wilfordii, the extracts of which have been used extensively in East Asia to treat various diseases including anti‑ischemic stroke. In the present study, the anti‑adherent activity of CA in lipopolysaccharide (LPS)‑stimulated human umbilical vascular endothelial cells (HUVECs) was investigated. CA markedly reduced the expression of vascular adhesion molecule‑1 (VCAM‑1) by LPS in HUVECs. The results also demonstrated that CA significantly reduced the expression of pro‑inflammatory and chemoattractant cytokines, including interleukin (IL)‑1β, IL‑6, IL‑8, monocyte chemoattractant protein‑1 and tumor necrosis factor‑α, in LPS‑activated human endothelial cells. CA inhibited the phosphorylation of mitogen‑activated protein kinases, including the extracellular signal‑regulated kinase 1/2 and p38 kinases. It was found that CA decreased the IKK/IκB‑α phosphorylation of inhibitor of nuclear factor (NF)‑κB kinase/inhibitor of NF‑κB‑α, suppressed translocation of the NF‑κB p65 subunit into the nucleus and inhibited the transcriptional activity of NF‑κB. CA also decreased human monocyte cell adhesion to endothelial cells in LPS‑stimulated conditions. These results demonstrated that CA inhibited the protein expression of VCAM‑1 and pro‑inflammatory cytokines by suppressing the transcriptional activity of NF‑κB. The results also suggested that CA may be important in the development of anti‑inflammatory drugs by inhibiting the expression of cell adhesion molecules.