Inhibition of STAT3 phosphorylation by sulforaphane reduces the lipopolysaccharide‐induced adhesion molecule expression in vascular endothelial cell

Intercellular adhesion molecule 1 (ICAM‐1) and vascular cell adhesion molecule 1 (VCAM‐1) play key roles in the initiation of vascular inflammation. In this study, we explored whether sulforaphane, a dietary phytochemical, can inhibit the expression of ICAM‐1 and VCAM‐1 in human umbilical vein endothelial cells (HUVEC) stimulated with lipopolysaccharide (LPS), and the mechanisms involved. Sulforaphane prevented the LPS‐mediated increase in ICAM‐1 and VCAM‐1 expression, ( P <0.01) in HUVEC. Sulforaphane also prevented the LPS‐mediated increase in the phosphorylation of signal transducer and activator of transcription 3 (STAT3) ( P <0.01). Stattic, a STAT3 inhibitor, reduced the LPS‐induced expression of ICAM‐1 and VCAM‐1, and STAT3 phosphorylation (P<0.01). STAT3 small interfering RNA treatment reduced the LPS‐induced expression of ICAM‐1, VCAM‐1 and STAT3 ( P <0.01). Sulforaphane reduced LPS‐mediated THP‐1 monocyte adhesion to HUVEC ( P <0.01). These data provide insight into the mechanism through which sulforaphane partly reduces the expression of ICAM‐1 and VCAM‐1 on the vascular endothelial cell by inhibiting STAT3 phosphorylation. Support or Funding Information This research was supported by Basic Science Research Program through the National Research Foundation of Korea(NRF) funded by the Ministry of Science, ICT & Future Planning(2012010913).