Effects of baicalin on the expression of TAFI,NF-κB,and ACE2 in the atherosclerotic rats / 重庆医学

Objective To explore the effects of baicalin on the expression of TAFI,NF-κB,and ACE2 in the atherosclerotic rats and discuss the anti-atherosclerosis mechanisms of baicalin.Methods The subjects were healthy male Wistar rats.The rats were divided into sham operation group,model group,baicalin high dose group (1 50 mg·kg-1 ·d-1 )and baicalin low dose group (100 mg·kg-1 ·d-1 ).Plasma TAFI activity were detected with enzymatic assays.The expression of NF-κB and ACE2 were detec-ted with immunohistochemical staining.Results Compared with sham group,the rest groups of TAFI and ACE2 activity were sig-nificantly higher (P <0.05),and the expression of NF-κB,had significant decreased (P <0.05).Compared with the model group, the level of TAFI and ACE2 in baicalin drug group was significantly lower than the model group (P <0.05),and the expression of NF-κB,had significant increased.Conclusion Baicalin can reduce TAFI and ACE2 level,and upregulate the expression of NF-κB to play its role in anti atherosclerosis.

The tendency of PAI-1 and TAFI levels in STEMI patients after thrombolytic treatment and its predictive value to restoration of coronary perfusion / 中华急诊医学杂志

Objective To observe the tendency of the plasma concentration of plasminogen activator inhibitor type-1 (PAI-1) and thrombin activatable fibrinolysis inhibitor (TAFI) before and after thrombolytic treatment of acute ST elevation myocardial infarction (STEMI) and to explore their recanalization predictive value of PAI-1 and TAFI for acute myocardial infarction patients with thrombolytic treatment.Methods Sixty patients,who received thromobolytic treatment from January 2007 to March 2009,were prospectively recruited.The blood sample were collected within 2 hours of thromobolytic treatment ( 0,0.5 h,1 h,1.5 h and 2 h).The plasma concentration of TAFI and PAI-1 were test by ELISA.16 healthy people were recruited as control group.Results The plasma levels of PAI-1 in STEMI patients before thrombolytic treatment were higher than those of Control group ( P ＜0.01 ),however the same significant change of TAFI level was not seen.The levels of TAFI were no significant difference before and after thrombolytic therapy during whole observation periods.However,the level of PAI-1 increased at 1.5 h and 2 h after thrombolytic therapy (P ＜ 0.01 ).The plasma PAI-1 levels of no - revascularigation group at 2 h after thrombolytic therapy were significant higher than that in revascularization group ( P ＜ 0.05 ).The levels of TAFI were not significantly different between two groups (P ＞ 0.05).Conclusions The decrease of plasma PAI-1 from high level within 2 hours after thrombolysis treament may be exploring the predictive value for revascularization.The tendency of TAFI can' t forecast the result of revascularization.

Elevated levels of activated and inactivated thrombin-activatable fibrinolysis inhibitor in patients with sepsis / 대한혈액학회지

BACKGROUND: In sepsis, large scale inflammatory responses can cause extensive collateral damage to the vasculature, because both coagulation and fibrinolysis are activated unevenly. Thrombin-activatable fibrinolysis inhibitor (TAFI) plays a role in modulating fibrinolysis. Since TAFI can be activated by both thrombin and plasmin, it is thought to be affected in sepsis. Hence, activated and inactivated TAFI (TAFIa/ai) may be used to monitor changes in sepsis. METHODS: TAFIa/ai-specific in-house ELISA can detect only the TAFIa/ai form, because the ELISA capture agent is potato tuber carboxypeptidase inhibitor (PTCI), which has selective affinity towards only the TAFIa and TAFIai isoforms. TAFIa/ai levels in plasma from 25 patients with sepsis and 19 healthy volunteers were quantitated with the in-house ELISA. RESULTS: We observed increased TAFIa/ai levels in samples from patients with sepsis (48.7+/-9.3 ng/mL) than in samples from healthy individuals (10.5+/-5.9 ng/mL). In contrast, no difference in total TAFI concentration was obtained between sepsis patients and healthy controls. The results suggest that TAFI zymogen was activated and that TAFIa/ai accumulated in sepsis. CONCLUSION: The detection of TAFIa/ai in plasma could provide a useful and simple diagnostic tool for sepsis. Uneven activation of both coagulation and fibrinolysis in sepsis could be caused by the activation of TAFI zymogen and elevation of TAFIa/ai. TAFIa/ai could be a novel marker to monitor sepsis and other blood-related disturbances.

The Significance of Thrombin Activable Fibrinolysis Inhibitor in Ischemic Stroke / 대한진단검사의학회지

BACKGROUND: Thrombin/thrombomodulin complex activates thrombin activable fibrinolysis inhibitor (TAFI) to active TAFI (TAFIa), which in turn catalyzes the hydrolysis of C-terminal lysine residues of partially degraded fibrin. The fibrin that is partially degraded by TAFIa is not degraded by plasmin. Thus, TAFI inhibits fibrinolysis. An increase in plasma TAFI level is suggested to be associated with thrombotic disorders. In this study, we measured TAFI levels and investigated the distribution of C+1542G polymorphism in Korean patients with ischemic stoke. And, we intended to investigated the role of TAFI in the occurrence of ischemic stroke. METHODS: We enrolled 44 patients who had experienced ischemic stroke episodes more than 6 month ago and had not been treated with oral anticoagulant. We also tested 44 age and sex-matched healthy controls. TAFI antigen levels were measured by an enzyme-linked immunosorbent assay (VisulizeTM TAFI antigen kit; Affinity Biologicals Inc., Ancaster, Canada) and TAFI activity levels were measured by a chromogenic assay (Actichrome TAFI activity kit ; American diagnostica Inc., CT, USA). Genotyping of C+1542G polymorphism was performed by an allele-specific polymerase chain reaction. RESULTS: The range of TAFI antigen was 2.4-12.7microgram/mL (mean+/-2SD) and that of TAFI activity was 4.9-17.9microgram/mL (mean+/-2SD) in healthy controls. TAFI antigen level was not correlated with TAFI activity. TAFI activity was the highest in CC polymorphism and the lowest in GG polymorphism (P= 0.03). The levels of TAFI antigen and activity were lower in the patients with ischemic stroke than in healty controls, but the difference was not statistically significant. There was no difference in the distribution of C+1542G polymorphism between the patients with ischemic stroke and healthy persons. CONCLUSIONS: In this study, TAFI antigen and activity were not significantly associated with the occurrence of ischemic stoke in Korean. And, TAFI may not be a risk factor for ischemic stroke in the Korean population.