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机构地区:[1]解放军总医院老年心内科,北京100853 [2]军事医学科学院放射研究所
出 处:《中华心血管病杂志》2002年第11期684-686,共3页Chinese Journal of Cardiology
摘 要:目的 探讨脂肪酸影响血管内皮细胞纤溶酶原激活物抑制剂 1表达的机制。方法 以PAI 1启动子控制表达氯霉素转移乙酰酶 (CAT)报告基因的重组质粒—PAI pCAT转染人血管内皮细胞株ECV30 4,并且部分共转染不同量的过氧化体增殖物激活型受体 (PPAR)α或PPARγ表达载体。分别以亚麻酸、亚油酸、油酸、硬脂酸诱导转染细胞 ,酶联免疫吸附方法测定CAT表达量显示启动子片段转录活性。结果 亚麻酸、亚油酸、油酸诱导以及增加PPARα表达可提高PAI 1启动子转录活性 ,硬脂酸诱导和增加PPARγ表达无影响。结论 不饱和脂肪酸可通过提高PAI 1转录活性诱导其在血管内皮细胞的表达 ,此作用涉及PPARα对PAI 1基因转录的诱导调节。Objective To investigate the mechanism of various fatty acids′ effect on plasminogen activator inhibitor -1 expression in human endothelial cells.Methods Cultured endothelial cell line-ECV304 was co-transfected with PAI-1 promoter controlled CAT reporter gene, and PPARα or PPARγ expression vetors. These cells were exposed to lionlenic acid, linoleic acid, oleic acid and stearic acid. The transcripton activity of PAI-1 promote was demonstrated as CAT expression termined by ELISA. Results Induction of lionlenic acid,linoleic acid, oleic acid and enhancing expression level of PPARα could increased transcription activity of PAI-1 promoter, while induction of stearic acid and enhancing espression of PPARγ had no major effect. Conclusion The unsaturated fatty acids can induce the expression of PAI-1 through promoting transcription activity of PAI-1 promoter in endothelial cells. PPARα plays an active role in this effect.
关 键 词:脂肪酸 血管内皮细胞 纤溶酶原激活抑制物1 过氧化体增殖物激活型受体
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