Abstract 223: Inhibition of STAT3 Phosphorylation by Sulforaphane Reduces Adhesion Molecule Expression in Vascular Endothelial Cell
This study explored the mechanism(s) by which sulforaphane inhibits intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) expressions stimulated with lipopolysaccharide (LPS) in human umbilical vein endothelial cell (HUVEC).
The protein levels of ICAM-1 and VCAM-1 were investigated by primary antibodies of anti-human ICAM-1, anti-human VCAM-1. The phosphorylation levels of signal transducer and activator of transcription 3 (STAT3) were investigated by phospho-STAT3 antibody. The STAT3-specific small interfering RNA (siRNA) was used to knockdown the expression of STAT3. THP-1 monocyte adhesion photograph images were obtained using a fluorescence microscope. Sulforaphane prevented LPS-mediated increase of ICAM-1 and VCAM-1 expression. Sulforaphane prevented LPS-mediated increase of STAT3 phosphorylation. AG490, Janus kinase (JAK)-2 inhibitor and Stattic, STAT3 inhibitor, reduced LPS-induced the expressions of ICAM-1 and VCAM-1, respectively. STAT3 small interfering RNA (siRNA) treatment reduced ICAM-1 and VCAM-1 expression stimulated with LPS. Sulforaphane reduced LPS-mediated THP-1 monocyte adhesion to HUVEC. These data provide a novel mechanism where sulforaphane decreases an expression of ICAM-1 and VCAM-1 onto vascular wall through an inhibition of STAT3 phosphorylation.
Author Disclosures: H.Y. Ahn: None. Y.S. Cho: None. C.H. Kim: None.
- © 2015 by American Heart Association, Inc.