Chlorophyll-related compounds inhibit cell adhesion and inflammation in human aortic cells

J Med Food. 2013 Oct;16(10):886-98. doi: 10.1089/jmf.2012.2558. Epub 2013 Sep 25.


The objectives of this study were to investigate the effects of chlorophyll-related compounds (CRCs) and chlorophyll (Chl) a+b on inflammation in human aortic endothelial cells. Adhesion molecule expression and interleukin (IL)-8, nuclear factor (NF)-κB p65 protein, and NF-κB and activator protein (AP)-1 DNA binding were assessed. The effects of CRCs on inflammatory signaling pathways of signal transducers and activators of transcription 3 (STAT3) and mothers against decapentaplegic homolog 4, respectively induced by IL-6 and transforming growth factor (TGF)-β, in human aortic smooth muscle cells cultured in vitro were also investigated. HAECs were pretreated with 10 μM of CRCs, Chl a+b, and aspirin (Asp) for 18 h followed by tumor necrosis factor (TNF)-α (2 ng/mL) for 6 h, and U937 cell adhesion was determined. TNF-α-induced monocyte-endothelial cell adhesion was significantly inhibited by CRCs. Moreover, CRCs and Chl a+b significantly attenuated vascular cell adhesion molecule-1, intercellular adhesion molecule-1, and IL-8 expressions. Treatments also significantly decreased in NF-κB expression, DNA binding, and AP-1 DNA binding by CRCs and Asp. Thus, CRCs exert anti-inflammatory effects through modulation of NF-κB and AP-1 signaling. Ten micromoles of CRCs and Asp upregulated the expression of mothers against decapentaplegic homolog 4 (Drosophila) (SMAD4) in the TGF-β receptor signaling pathway, and SMAD3/4 transcription activity was also increased. Ten micromoles of CRCs were able to potently inhibit STAT3-binding activity by repressing IL-6-induced STAT3 expression. Our results provide a potential mechanism that explains the anti-inflammatory activities of these CRCs.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aorta / cytology
  • Aorta / drug effects*
  • Aorta / immunology*
  • Atherosclerosis / drug therapy
  • Atherosclerosis / genetics
  • Atherosclerosis / immunology*
  • Atherosclerosis / physiopathology
  • Cell Adhesion / drug effects*
  • Chlorophyll / pharmacology*
  • Down-Regulation / drug effects
  • Endothelial Cells / cytology
  • Endothelial Cells / drug effects
  • Endothelial Cells / immunology
  • Humans
  • Intercellular Adhesion Molecule-1 / genetics
  • Intercellular Adhesion Molecule-1 / immunology
  • Interleukin-6 / genetics
  • Interleukin-6 / immunology
  • Interleukin-8 / genetics
  • Interleukin-8 / immunology
  • NF-kappa B / genetics
  • NF-kappa B / immunology
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / immunology
  • U937 Cells


  • Interleukin-6
  • Interleukin-8
  • NF-kappa B
  • Tumor Necrosis Factor-alpha
  • Intercellular Adhesion Molecule-1
  • Chlorophyll