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目的:探讨动脉粥样硬化兔脂肪组织组织因子(TF)和Ⅰ型纤溶酶原激活物抑制剂(PAI-1)表达及非诺贝特对其的影响。方法:15只兔随机等分为3组,正常组予普通饲料喂养12周,动脉粥样硬化组给予高胆固醇饮食12周,非诺贝特组在高胆固醇饮食8周后加非诺贝特30mg·kg-1·d-1干预4周。实验第12周末取兔皮下脂肪组织,RT-PCR测定脂肪组织TF和PAI-1mRNA表达;同时采血10ml,分离血浆,用ELISA方法测定血浆TF活性,发色底物法测定血浆PAI-1活性。结果:高胆固醇饮食可显著升高血清总胆固醇(TC)(P<0·05),血清三酰甘油(TG)无明显升高;加用非诺贝特治疗4周,TC和TG均无明显改变。动脉粥样硬化组脂肪组织TF和PAI-1mRNA表达(分别为1.15±0.01和1.20±0.01)明显高于正常组(分别为1.03±0.01和1.10±0.01),均P<0·01;血浆TF和PAI-1活性[分别为(74.4±28.8)ng/L和(15.6±1.9)×103AU/L]较正常组[分别为(33.1±10.7)ng/L和(6.9±0.9)×103AU/L]增高(P<0·05)。非诺贝特组TF和PAI-1mRNA表达(分别为1.02±0.01和1.06±0.01)、血浆TF和PAI-1活性[分别为(40.3±12.2)ng/L和(7.5±1.5)×103AU/L]均有显著降低(P<0.01或P<0·05)。结论:动脉粥样硬化兔脂肪组织表达TF和PAI-1增加,活性增强,非诺贝特能抑制动脉粥样硬化兔脂肪组织TF和PAI-1的表达及活性,提示非诺贝特可能具有独立于降脂作用之外的抗血栓作用。
Objective: To investigate the effect of fenofibrate on the expression of adipose tissue factor (TF) and type Ⅰ plasminogen activator inhibitor (PAI-1) in atherosclerotic rabbits. Methods: Fifteen rabbits were randomly divided into three groups: normal group fed with normal diet for 12 weeks, atherosclerosis group given high cholesterol diet for 12 weeks, fenofibrate group fed fenofibrate 30mg · kg-1 · d-1 for 4 weeks. At the end of the twelfth week, the subcutaneous adipose tissue of rabbit was taken and the expression of TF and PAI-1 mRNA in adipose tissue was determined by RT-PCR. At the same time, 10 ml of blood was collected to separate the plasma. The plasma TF activity was measured by ELISA. PAI-1 activity was measured by chromogenic substrate method. Results: High cholesterol diet significantly increased serum total cholesterol (TC) (P0.05), serum triglyceride (TG) did not increase significantly; with fenofibrate treatment for 4 weeks, TC and TG were no Significant change. The expression of TF and PAI-1mRNA in adipose tissue of atherosclerosis group (1.15 ± 0.01 and 1.20 ± 0.01 respectively) were significantly higher than that of normal group (1.03 ± 0.01 and 1.10 ± 0.01 respectively), both P <0.01; And PAI-1 activity (74.4 ± 28.8 ng / L and 15.6 ± 1.9 × 103 AU / L, respectively) were significantly higher than those in the normal group [33.1 ± 10.7 ng / L and 6.9 ± 0.9 × 103 AU / L] increased (P <0 · 05). TF and PAI-1 mRNA expression in fenofibrate group (1.02 ± 0.01 and 1.06 ± 0.01, respectively) and plasma TF and PAI-1 activity (40.3 ± 12.2 ng / L and 7.5 ± 1.5 × 103 AU / L] were significantly lower (P <0.01 or P <0.05). Conclusion: The expression of TF and PAI-1 in atherosclerotic rabbits increased and the activity was enhanced. Fenofibrate could inhibit the expression and activity of TF and PAI-1 in atherosclerotic rabbit adipose tissue, suggesting that fenofibrate might have Independent of anti-thrombotic effects other than lipid-lowering effects.