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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Nafamostat mesilate suppresses NF-kappaB activation and NO overproduction in LPS-treated macrophages.

Nafamostat mesilate (NM), a clinically used serine protease inhibitor, suppressed the overproduction of nitric oxide (NO) and the expression of inducible nitric oxide synthase ( iNOS) in RAW264.7 murine macrophages treated with lipopolysaccharide ( LPS, 100 ng/ml); however, it had little effect on endothelial NOS ( eNOS) in human umbilical vein endothelial cells (HUVEC). Electrophoretic mobility shift assay (EMSA) revealed that LPS activated nuclear factor-kappaB (NF-kappaB) in RAW264.7 cells and that this activation was suppressed by nafamostat mesilate. Western blotting showed that nafamostat mesilate suppressed the phosphorylation and degradation of inhibitor kappaB-alpha (IkappaB-alpha), which holds NF-kappaB in the cytoplasm in an inactivated state. Our observations suggest that nafamostat mesilate is a candidate agent for various diseases such as ischemia-reperfusion, graft rejection, inflammatory diseases, and autoimmune diseases, in which iNOS and/or NF-kappaB are upregulated.[1]

References

  1. Nafamostat mesilate suppresses NF-kappaB activation and NO overproduction in LPS-treated macrophages. Noguchi, S., Nakatsuka, M., Konishi, H., Kamada, Y., Chekir, C., Kudo, T. Int. Immunopharmacol. (2003) [Pubmed]
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