META060 attenuates TNF-α-activated inflammation, endothelial-monocyte interactions, and matrix metalloproteinase-9 expression, and inhibits NF-κB and AP-1 in THP-1 monocytes.
Atherosclerosis
; 223(1): 130-6, 2012 Jul.
Article
in En
| MEDLINE
| ID: mdl-22658256
ABSTRACT
BACKGROUND:
Cytokine-induced monocyte-endothelial interaction and vascular inflammation play a critical role in atherogenesis. A modified hop extract, META060, was identified as an inhibitor of inflammatory mediators in human rheumatoid arthritis synovial fibroblasts.OBJECTIVE:
To determine how META060 may impact the initial stages of atherosclerosis, we investigated the effects of META060 in endothelial and monocyte cell models.METHODS:
andresults:
TNF-α (10 ng/mL)-activated human monocytic THP-1 cells adhered to human aortic endothelial cells (HAECs); pre-treatment of cells with META060 (10 µg/mL) significantly inhibited cell adhesion. META060 (1-20 µg/mL) inhibited TNF-α-induced expression of inflammatory mediators including IL-1ß, MCP-1 and RANTES in HAECs and THP-1 cells. TNF-α- or LPS-mediated MMP-9 protein levels (measured by an immunoassay) and enzyme activity (determined by zymography) were inhibited by META060 in a dose-dependent manner. Data from transcription factor screening assays showed that META060 selectively inhibited NF-κB and AP-1 in THP-1 cells, suggesting that META060 regulated inflammatory markers through gene regulation.CONCLUSION:
META060 inhibited monocyte-endothelial cell interactions and suppressed multiple biomarkers of inflammation in both a monocytic cell line and an endothelial cell line. MMP-9 expression and activity also were inhibited. These effects resulted in part from META060's inhibition of transcription factors NF-κB and AP-1. META060 may have beneficial effects for prevention or treatment of cardiovascular diseases by ameliorating inflammation and plaque destabilization, which are hallmarks of atherosclerosis.
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Plant Extracts
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Monocytes
/
Cell Communication
/
NF-kappa B
/
Tumor Necrosis Factor-alpha
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Transcription Factor AP-1
/
Inflammation Mediators
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Humulus
/
Endothelial Cells
/
Matrix Metalloproteinase Inhibitors
Type of study:
Prognostic_studies
Limits:
Humans
Language:
En
Journal:
Atherosclerosis
Year:
2012
Document type:
Article
Affiliation country: