Abstract

OBJECTIVESWe investigated whether curcumin, an ingredient of turmeric, can suppress the expression of intercellular adhesion molecule 1 (ICAM‐1) and vascular cell adhesion molecule 1 (VCAM‐1) in human umbilical vein endothelial cells (HUVEC) stimulated with lipopolysaccharide (LPS), and the underlying mechanisms.MATERIALS AND METHODOLOGYThe levels of adhesion molecules, activities of nuclear factor kappaB (NF‐kB) and signal transducer and activator of transcription 3 (STAT3) were determined using Western blot analysis. The effect of curcumin on monocyte binding to endothelial cells was determined using THP‐1 monocyte (human acute monocytic leukemia cell line) adhesion assay.RESULTSCurcumin prevented the LPS‐mediated increase in ICAM‐1 and VCAM‐1 expression in HUVEC in a dose‐dependent manner. Curcumin did not affect LPS induced degradation of IkappaBα (IkBα). On the other hand, curcumin reduced the LPS‐induced STAT3 phosphorylation. Curcumin significantly reduced LPS‐mediated THP‐1 monocyte adhesion to HUVEC. Furthermore, in C57BL/6 mice, curcumin prevented the LPS induced increase in aortic ICAM‐1 and VCAM‐1 expression.CONCLUSIONSCurcumin prevented LPS‐induced ICAM–1 and VCAM–1 expression on vascular endothelial cells associated with inhibition of STAT3 phosphorylation.Support or Funding InformationThis work was supported by the research grants of the Chungbuk National University in 2014.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

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