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目的 探讨动脉粥样硬化兔脂肪细胞I型纤溶酶原激活物抑制剂 (PAI-1)表达及非诺贝特对其影响。方法 15只兔随机分为三组 ,正常组予普通饲米喂养 ,对照组给以高胆固醇饮食 ,实验组在高胆固醇饮食 8周后加用非诺贝特干预 4周。RT -PCR测定脂肪细胞PAI-mRNA表达 ;发色底物法测定血浆PAI -1活性。结果 高胆固醇饮食显著升高血清总胆固醇 (TC) (P <0 0 0 0 1) ,血清甘油三酯 (TG)无明显升高 ;非诺贝特治疗后 ,TC和TG均无明显降低。对照组脂肪细胞PAI -mRNA表达为 1 12 9± 0 0 12 ,血浆PAI-1活性为 (15 6± 1 9)× 10 3 AU/L ,均明显高于正常组的 1 0 10± 0 0 2 0和 (6 9± 0 9)× 10 3 AU/L(P <0 0 1) ;研究组PAI -mRNA表达(1 0 2 3± 0 0 2 3 )和活性 [(7 5± 1 5 )× 10 3 AU/L]均较研究对照组显著降低 (P <0 0 1)。结论 对照组兔脂肪细胞表达PAI -1明显增加 ,活性增强 ;非诺贝特能抑制动脉粥样硬化兔脂肪细胞PAI -1的表达 ,降低PAI-1活性 ,提示非诺贝特可能具有独立于降脂外的抗血栓作用。
Objective To investigate the expression of type Ⅰ plasminogen activator inhibitor (PAI-1) in atherosclerotic rabbit’s adipocytes and the effect of fenofibrate on it. Methods Fifteen rabbits were randomly divided into three groups. The normal group was fed with normal diet. The control group was given high cholesterol diet. The experimental group was treated with fenofibrate for 8 weeks after high cholesterol diet for 4 weeks. The expression of PAI-mRNA in adipocytes was determined by RT-PCR and the PAI-1 activity in plasma was determined by chromogenic substrate method. Results High cholesterol diet significantly increased serum total cholesterol (TC) (P <0.01 01), serum triglyceride (TG) did not increase significantly; fenofibrate treatment, TC and TG were not significantly reduced. PAI-mRNA expression of adipocytes in control group was 1 12 9 ± 0 0 12 and plasma PAI-1 activity was (15 6 ± 1 9) × 10 3 AU / L, both of which were significantly higher than those of normal group PAI-mRNA expression (10 02 3 ± 0 0 2 3) and activity [(7 5 ± 1 5)] in the study group were significantly higher than those in the control group (P <0.01) ) × 10 3 AU / L] were significantly lower than the control group (P <0.01). CONCLUSION: The expression of PAI-1 in adipocytes of control group is significantly increased and its activity is enhanced. Fenofibrate can inhibit the expression of PAI-1 in adipocytes of atherosclerotic rabbits and decrease the activity of PAI-1, suggesting that fenofibrate might be independent of Anti-thrombotic effects outside of lipid.