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目的:观察氧化型低密度脂蛋白对人平滑肌细胞核因子κB激活的影响,探讨氧化型低密度脂蛋白致动脉粥样硬化机制。方法:以体外培养的人脐动脉平滑肌细胞为对象,采用免疫细胞化学法测定氧化型低密度脂蛋白与核因子κB亚单位p65核移位的时间效应与浓度效应关系。结果:在氧化型低密度脂蛋白刺激下,平滑肌细胞中0.5h即出现核因子κB核移位,2h达高峰,4h仍持续可见。不同浓度(12.5,25,50及100mg/L)氧化型低密度脂蛋白均可诱导平滑肌细胞中核因子κB核移位,在一定剂量范围内,氧化型低密度脂蛋白的浓度越大,核因子κB核移位越明显,尤以50mg/L的氧化型低密度脂蛋白作用最明显。结论:氧化型低密度脂蛋白可刺激平滑肌细胞中核因子κB的激活,进一步提示氧化型低密度脂蛋白/核因子κB信号途径在促进动脉粥样硬化发病机制中起重要作用。
Objective: To investigate the effect of oxidized low density lipoprotein on activation of nuclear factor κB in human smooth muscle cells and to explore the mechanism of oxidative low density lipoprotein induced atherosclerosis. Methods: Human umbilical artery smooth muscle cells (VSMCs) were cultured in vitro. The relationship between the time effect of oxidative low density lipoprotein and the nuclear translocation of NF-κB subunit p65 was studied by immunocytochemistry. Results: In oxidative low density lipoprotein (LDL) stimulation, NF-κB nuclear translocation appeared in smooth muscle cells at 0.5h, peaked at 2h and remained visible at 4h. Different concentrations of (12.5, 25, 50 and 100 mg / L) oxidized low density lipoprotein can induce NF-κB nuclear translocation in smooth muscle cells. The concentration of oxidized low density lipoprotein κB nuclear translocation more obvious, especially in the role of oxidized low density lipoprotein 50mg / L most obvious. CONCLUSION: Oxidized low density lipoprotein (LDL) can stimulate the activation of nuclear factor kappa B in smooth muscle cells, further suggesting that oxidized low density lipoprotein / nuclear factor kappa B signaling plays an important role in the pathogenesis of atherosclerosis.