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Nicotinamide inhibits endotoxin-induced monocyte tissue factor expression.
J S Ungerstedt1, K Heimersson, T Söderström
1Coagulation Research, Department of Surgical Sciences,Karolinska Hospital, Karolinska Institutet, Stockholm, Sweden. johanna.ungerstedt@ks.se
Journal of Thrombosis and Haemostasis : JTH
|December 17, 2003
Summary
Nicotinamide effectively inhibits endotoxin-induced blood coagulation activation by reducing tissue factor (TF) and IL-6. This vitamin B derivative shows therapeutic potential for inflammatory and thrombotic conditions like sepsis.
Area of Science:
- Biochemistry
- Immunology
- Hematology
Background:
- Tissue factor (TF) initiates blood coagulation in vivo.
- Increased monocyte TF expression is linked to thrombotic complications in sepsis and DIC.
Purpose of the Study:
- To investigate the effect of nicotinamide on endotoxin-induced monocyte TF and CD11b expression, IL-6, and clotting onset time (COT).
Main Methods:
- Experiments utilized human peripheral blood leukocyte suspensions and whole blood from healthy volunteers.
- Free oscillating rheometry and flow cytometry assessed endotoxin's impact on TF, CD11b, IL-6, and coagulation.
Main Results:
- Endotoxin increased IL-6, TF, and CD11b expression, shifting COT towards procoagulation.
- Nicotinamide (4 mmol/L) inhibited TF expression, IL-6, and normalized COT; higher concentrations (16 mmol/L) further reduced CD11b.
- Monocyte TF expression correlated with COT, and TF blockade inhibited the procoagulant shift.
Conclusions:
- Nicotinamide demonstrates efficacy in inhibiting coagulation activation during endotoxemia.
- Nicotinamide's anti-inflammatory properties suggest therapeutic potential in diseases with high coagulation and inflammation, such as sepsis and DIC.