Aim To study the effect of anisodamine on lipopolysaccharide (LPS) induced expression of tissue factor (TF) in vascular endothelial cells (EC). Methods Human umbilical vein endothelial cells (hUVEC) were cultured by trypsin digestion method. TF activity was measured in the lysates of hUVEC by using a single step clotting assay. Specific mRNA expressions were determined by Northern blotting. In order to evaluate a possible contribution of the nuclear factor κB (NF κB) pathway on anisodamine effects, electrophoretic mobility shift assays (EMSA) were performed using nuclear extracts from hUVEC and NF κB binding oligonucleotides. Results Treatment of hUVEC with LPS resulted in a significant increase in TF activity. Anisodamine dose dependently inhibited LPS induced upregulation of TF. These effects were also confirmed on the level of specific TF mRNA expression by Northern blotting. Furthermore, anisodamine completely abolished LPS induced NF κB DNA binding activity in nuclear extracts from hUVEC treated with LPS together with anisodamine. Conclusions Anisodamine counteracts endothelial cell activation by inhibiting LPS induced TF expression in these cells. Its interference with the NF κB pathway might at least partly contribute to this effect. The ability of anisodamine to counteract the effect of LPS on endothelial cells might be one underlying mechanism explaining its antithrombosis and efficacy in the treatment of bacteraemic shock.