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Updated: Oct 13, 2026
Culture of Macrophage Colony-stimulating Factor Differentiated Human Monocyte-derived Macrophages
Published on: June 30, 2016
Vitamin C suppresses lipopolysaccharide-induced procoagulant response of human monocyte-derived macrophages
M S Parahuleva1, J Jung, M Burgazli
1Internal Medicine/Cardiology and Angiology, University Hospital of Giessen and Marburg, Giessen, Germany. mariana.parahuleva@innere.med.uni-giessen.de.
Insights
Vitamin C reduces inflammation and clotting factors in immune cells, offering potential cardiovascular benefits beyond its antioxidant effects. This study clarifies vitamin C
Area of Science:
- Vascular Biology
- Immunology
- Biochemistry
Background:
- Epidemiological evidence for vitamin C's role in cardiovascular disease prevention is inconsistent.
- Vitamin C is a known antioxidant, but its specific mechanisms in vascular pathophysiology require further definition.
Purpose of the Study:
- To investigate the effect of vitamin C on tissue factor (TF) and Factor VII Activating Protease (FSAP) expression.
- To determine vitamin C's influence on NF-kB activity in human monocyte-derived macrophages stimulated by lipopolysaccharide (LPS) and reactive oxygen species (ROS).
Main Methods:
- Human monocyte-derived macrophages were treated with clinically relevant doses of vitamin C.
- The study examined the impact of vitamin C on LPS- and ROS-induced NF-kB activation, including IkBa phosphorylation and degradation.
- Expression levels of TF and FSAP were measured following vitamin C treatment.
Main Results:
- Vitamin C inhibited LPS- and ROS-induced NF-kB DNA-binding activity in a concentration-dependent manner.
- Vitamin C reduced the phosphorylation and degradation of the inhibitor protein IkBa.
- Vitamin C decreased the expression of TF and FSAP, key mediators of inflammation and coagulation.
Conclusions:
- Vitamin C modulates pro-inflammatory and pro-coagulatory pathways by inhibiting NF-kB activation.
- Vitamin C demonstrates beneficial antiatherogenic effects on human monocyte-derived macrophages, complementing its antioxidant properties.
Objective:
Although vitamin C is a strong antioxidant, the epidemiologic evidence to support its role in lowering risk of cardiovascular disease is inconsistent. In order to define the role of vitamin C in vascular pathophysiology, we have investigated the effect of vitamin C on the tissue factor (TF) and Factor VII Activating Protease (FSAP) expression induced by lipopolysaccharide (LPS) in human monocyte-derived macrophages.
Materials And Methods:
Vitamin C at clinically relevant doses was tested to its ability to influence the LPS- and reactive oxygen species (ROS) - generating system of xanthine/xanthine oxidase (X/XO) NF-kB activity in human monocyte-derived macrophages.
Results:
Vitamin C-treatment prevents LPS- and ROS-induced DNA-binding activity of NF-kB in a concentration-dependent fashion. Vitamin C also inhibited the phosphorylation and proteolytic degradation of the inhibitor protein IkBa. In parallel to regulate NF-kB activity, vitamin C reduced the expression of TF and FSAP, genes known to be induced by bacterial LPS and triggered the extrinsic coagulation cascade and linked thrombosis with inflammation.
Conclusions:
Vitamin C alters pro-inflammatory and pro-coagulatory processes via inhibition of NF-kB activation and exerts beneficial antiatherogenic effects on human monocyte-derived macrophages in addition to its anti-oxidant properties.
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