Investigation Of TAFI Level And Mechanism Of Action In The Process Of Atherosclerosis In Rats.

Background: Coronary atherosclerotic heart disease(CHD) is a kind of global disease. and it does harm to mankind severity, which because of atherosclerosis induce organ deformed . Now not only it theats life and health of mankind in the developed contries, but also in our contry it is a severity challenge. Atherosclerosis is capital pathological and physiological foundation of CHD, then genesis development prevention and therapy of atherosclerosis have become a hot spot of research. And in the domain new discovery and new breakthrough uauslly appear . recently, in the cardiovascular and cerebrovascular diseases, ajustment of thrombosis and fibrinolysis may correlate with new biological factor, thrombin-activatable fibrinolysis Inhibitor (TAFI) has attached more importance as a factor regulatory to activity of thrombosis and fibrinolysis in cardiovascular and cerebrovascular diseases.Therefore, we propose to adopt conditions controlled scientific and severe animal experiment to identify the adjustment of thrombin-activatable fibrinolysis Inhibitor in the system of thrombosis and fibrinolysis. The breakthrough in the domain will provide new pathway and theroy foundation in the prevention and cure of atherosclerosis. Degrading TAFI level and using TAFI antagon will new methods in the prevention and cure of atherosclerosis, and advance to develop fibrinolysis drugs. These can generate great econimic and social efficiency to prevente and cure atherosclerosis. All mentioned above formed the objectives. Objective: The aim of this study is to investigate the level of TAFI andmechanism of action in the atherosclerosis.Methods: Totally 40 healthy male Wistar rats were randomly divided into 4 groups(n=10) ,controls group, high lipid group, high lipid +vitamin D overload group, endothelium injure group .four different feeding methods, including normal diet, hign lipid, hign lipid+vitamin D overload, and high lipid + vitamin D overload + endothelium injury, were used for inducing three stages of AS in rats. Then we measured PT APTT Fib, measured the activity of TAFI by a chromogenic assay.Results: (1) We use three means to copied three stages including high lipid,, hign lipid+vitamin D overload, and high lipid + vitamin D overload + endothelium injury, and the atherosclerosis model of the rats can be copied after four months. (2)TC TG LDL-C Fib and the activity level of TAFI in plasma of three model groups increased gradually compared with the controls (P<0.01) . HDL-C PT 和 APTT in plasma of three model groups decreased gradually compared with the controls (P <0.01or P<0.05) .(3)And the activity level of TAFI in plasma had positive relation with TG TC and Fib.Conclusions :1. We use three means to copied three stages including high lipid,, hign lipid+vitamin D overload, and high lipid + vitamin D overload + endothelium injury, and the atherosclerosis model of the rats can be copied after four months. 2.the activity level of TAFI in plasma has close relation with atherosclerosis severity, which indicates that TAFI is one of etiological factors of atherosclerosis.