Effects of tetramethylpyrazine on thrombin-induced tissue factor expression in vascular endothelial cells / 南方医科大学学报

<p><b>OBJECTIVE</b>To observe the effects of tetramethylpyrazine (TMP) on tissue factor (TF) expression induced by thrombin in human umbilical vein endothelium derived cell line ECV304.</p><p><b>METHODS</b>The changes in the total cellular procoagulant activity (PCA) of ECV304 cells exposed to thrombin were observed with one-stage clotting assay. TF mRNA expression in the exposed cells was examined using semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR).</p><p><b>RESULTS</b>ECV304 cells stimulated with increasing concentrations of thrombin (1.25-20 U/ml) showed a gradual increase of PCA (r=0.9602, P<0.01). The application of FVII-deficient plasma and the monoclonal antibody of TF confirmed that the PCA of the cells mediated by TF activity. TMP at 125-1000 microg/ml alone did not affect TF expression in ECV304 cells (P>0.20), TMP administered 30 min prior to thrombin exposure showed a significant concentration-dependent inhibitory effect on the increments of PCA (r=-0.9644, P<0.01) and TF mRNA expression (r=-0.9576, P<0.05) in ECV304 cells, and 1000 microg/ml TMP produced the strongest effect. In ECV304 cells stimulated with thrombin for 4, 6, 8, 10 and 12 h, TMP administration significantly inhibited the thrombin-induced PCA, and the effect was especially obvious at 8 h following thrombin exposure (P<0.05).</p><p><b>CONCLUSION</b>Thrombin induces TF expression in vascular endothelial cells, and this effect can be inhibited by TMP at the mRNA level.</p>

Value of plasma tissue factor, tissue factor pathway inhibitor and factor VII assessments in patients with acute myocardial and cerebral infarction / 南方医科大学学报

<p><b>OBJECTIVE</b>To study the clinical implications of changes in plasma tissue factor (TF), tissue factor pathway inhibitor (TFPI) and factor VII (FVII) after the onset of acute myocardial infarction (AMI) and acute cerebral infarction (ACI).</p><p><b>METHODS</b>Sixty-nine patients with AMI, 71 with ACI and 50 age-matched healthy volunteers were enrolled in this study. Blood samples were obtained from the healthy subjects and from the patients at the early stage of AMI and ACI onset for examination of plasma TF and TFPI activity using chromogenic assay, and the plasma TF and TFPI antigens were measured by enzyme-linked immunosorbent assay (ELISA). The plasma FVII coagulation activity (FVII:C) was also measured, and the plasma FVIIa determined using soluble TF assay.</p><p><b>RESULTS</b>Compared with the healthy control group, AMI patients had significantly enhanced plasma TF and TFPI activities and elevated TF and TFPI antigen levels (P<0.05), with also markedly increased FVIIa (P<0.05) but comparable FVII:C (P>0.05). In ACI patients, the plasma TF activity and antigen were obviously increased in comparison with the control group (P<0.05), but plasma TFPI activity and antigen were lowered (P<0.05), and both the FVII:C and FVIIa were markedly higher (P<0.05). Significant differences were noted in plasma TF and TFPI activities and their antigen levels as well as in FVII:C, but not in FVIIa between AMI and ACI patients.</p><p><b>CONCLUSION</b>V Following the onset of AMI and ACI, TF pathway is initiated and the risk of thrombogenesis increases, and the assessment of TF pathway is therefore of value for understanding the development of the condition.</p>