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氧化型脂蛋白(a)对人脐静脉内皮细胞表达巨噬细胞炎性蛋白1α的影响 被引量:2

Oxidized Lipoprotein(a) Enhanced the Expression of Macrophage Inflammatory Protein-1α in Cultured Human Umbilical Vein Endothelial Cells
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摘要 探讨氧化型脂蛋白 (a)能否诱导人脐静脉内皮细胞表达巨噬细胞炎性蛋白 1α ,以阐明其在动脉粥样硬化发生中的作用。在内皮细胞培养基中分别加入天然脂蛋白 (a)及不同浓度的氧化型脂蛋白 (a) ,采用细胞酶联免疫检测巨噬细胞炎性蛋白 1α蛋白的表达 ,用一步法提取RNA ,逆转录聚合酶链反应检测巨噬细胞炎性蛋白 1αmR NA的表达 ,并用单核细胞粘附率试验检测单核细胞粘附。结果发现 ,氧化型脂蛋白 (a)呈剂量依赖性增加内皮细胞巨噬细胞炎性蛋白 1α蛋白表达 ,5、10及 2 0nmol/L氧化型脂蛋白 (a)分别使巨噬细胞炎性蛋白 1α表达明显增加到12 1%± 8%、16 3%± 13%及 2 4 1%± 2 8%。氧化型脂蛋白 (a)促使单核细胞粘附率增加 ,并且粘附率与氧化型脂蛋白 (a)浓度呈正相关。且氧化型脂蛋白 (a)能促使巨噬细胞炎性蛋白 1αmRNA表达明显增加。结果提示 ,氧化型脂蛋白 (a)能诱导内皮细胞巨噬细胞炎性蛋白 1α表达增强 ,这可能与脂蛋白 (a) Aim To investigate the effects of oxidized lipoprotein (a) [ox-Lp(a)] on the expression of macrophage inflammatory protein-1α (MIP-1α)in cultured human umbilical endothelial cells (hUVEC). Methods Native Lp(a)[n-Lp(a)] and different concentrations of ox-Lp(a) were incubated with hUVEC. Cell ELISA was used to detect the expression of MIP-1α. Monocyte adhesion assay was used to detect the Monocyte adhesion. MIP-1α mRNA expression were determined by reverse transcriptase-polymerase chain reaction (RT-PCR). Results Ox-Lp(a) dramatically enhanced the levels of MIP-1α in a dose dependent manner, increasing MIP-1α epression in hUVEC by 121%±8% at 5 nmol/L,163%±13% at 10 nmol/L and 241%±28%at 20 nmol/L. In addition, 10 nmol/L of ox-Lp(a) for 2 h could significantly increase the amount of monocyte adherence to endothelial cells. Moreover, RT-PCR analysis demonstrated that the amount of MIP-1α mRNA increased after treatment with ox-Lp(a) for 24 h. Conclusion Ox-Lp(a) can induce MIP-1α expression in hUVEC, which may thereby influence the pathogenesis of athersclerosis.
出处 《中国动脉硬化杂志》 CAS CSCD 2004年第5期556-558,共3页 Chinese Journal of Arteriosclerosis
关键词 细胞生物学 氧化型脂蛋白(a)对内皮细胞表达巨噬细胞炎性蛋白1α的影响 细胞酶联免疫 化型脂蛋白(a) 巨噬细胞炎性蛋白1Α 人脐静脉内皮细胞 动脉粥样硬化 Oxidized Lipoprotein(a) Macrophage Inflammatory Protein-1α Human Umbilical Vein Endothelial Cells Atherosclerosis Monocyte Adhesion Reverse Transcriptase-Polymerase Chain Reaction
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参考文献11

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二级参考文献11

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