Format

Send to

Choose Destination
J Med Food. 2016 Jul;19(7):663-9. doi: 10.1089/jmf.2016.0030. Epub 2016 May 20.

Inhibition of TNF-α, IL-1α, and IL-1β by Pretreatment of Human Monocyte-Derived Macrophages with Menaquinone-7 and Cell Activation with TLR Agonists In Vitro.

Author information

1
1 Hubei Key Laboratory of Economic Forest Germplasm Improvement and Resources Comprehensive Utilization, College of Life Science, Huanggang Normal University , Hubei, China .
2
2 Department of Medical Research, China Medical University Hospital, China Medical University , Taichung, Taiwan .
3
3 Department of Health and Nutrition Biotechnology, Asia University , Taichung, Taiwan .
4
4 Institute of Food Sciences and Technology, National Taiwan University , Taipei, Taiwan .
5
5 The International Science and Health Foundation , Krakow, Poland .
6
6 Department of Food Science, Rutgers University , New Brunswick, New Jersey, USA.
7
7 Medical Institute of the State College of Computer Science and Business Administration , Łomża, Poland .
8
8 Department of Pediatric Orthopedics, Medical University of Białystok , Białystok, Poland .
9
9 Viridis BioPharma Private Limited , Mumbai, India .
10
10 Creighton University Medical Center , Omaha, Nebraska, USA.
11
11 American Medical Holdings Incorporated , New York, New York, USA.
12
12 NattoPharma ASA , Oslo, Norway .

Abstract

Circulatory markers of low-grade inflammation such as tumor necrosis factor-alpha (TNF-α), interleukin-1 alpha (IL-1α), and interleukin-1 beta (IL-1β) positively correlate with endothelial damage, atheroma formation, cardiovascular disease, and aging. The natural vitamin K2-menaquinone-7 (MK-7) added to the cell culture of human monocyte-derived macrophages (hMDMs) at the same time as toll-like receptor (TLR) agonists did not influence the production of TNF-α. When the cells were pretreated up to 6 h with MK-7 before treatment with TLR agonists, MK-7 did not inhibit significantly the production of TNF-α after the TLR activation. However, 30 h pretreatment of hMDMs with at least 10 μM of MK-7 effectively and dose dependently inhibited the proinflammatory function of hMDMs. Pretreatment of hMDMs with 10 μM of MK-7 for 30 h resulted in 20% inhibition of TNF-α production after lipopolysaccharide (LPS) activation (P < .05) and 43% inhibition after macrophage-activating lipopeptide (MALP) activation (P < .001). Pathogen-associated molecular pattern (PMPP) activation was inhibited by 20% with MK-7 pretreatment; however, this inhibition was not statistically significant. The 30 h pretreatment of a THP-1-differentiated monocyte cell line with MK-7 resulted in a dose-dependent downregulation of TNFα, IL-1α, and IL-1β gene expression as evaluated by RNA semiquantitative reverse transcription polymerase chain reaction (RT-PCR). MK-7 is able to modulate immune and inflammatory reactions in the dose-response inhibition of TNF-α, IL-1α, and IL-1β gene expression and protein production by the healthy hMDMs in vitro.

KEYWORDS:

MenaQ7® Crystals; TNF-α; cardiovascular; inflammation; menaquinone-7

PMID:
27200471
DOI:
10.1089/jmf.2016.0030
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Atypon
Loading ...
Support Center