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目的:探讨反式脂肪酸(TFAs)在ECV304细胞氧化低密度脂蛋白(LDL)过程中的作用,并揭示其作用机制。方法:利用实时荧光定量PCR的方法检测经反式脂肪酸刺激的ECV304细胞中HNP-1的表达;并通过流式细胞仪检测ECV304细胞中氧自由基的生成量以及ECV304细胞的凋亡情况;用脂质氧化产物丙二醛(MDA)生成量描述ECV304细胞对LDL氧化能力的变化。结果:经反式脂肪酸刺激ECV304细胞产生MDA的量(nmol/mg)明显增多(0.155±0.025,P<0.05),对LDL的氧化增强;反式脂肪酸刺激后ECV304细胞的胞内HNP-1表达水平升高(0.429±0.090,P<0.05),同时氧自由基水平也显著增加(66.700±6.532,P<0.05);钙离子拮抗剂的使用可以拮抗上述作用。结论:反式脂肪酸可能通过促进HNP-1的表达提高ECV304细胞氧化LDL的能力,这种氧化能力的提高可能与钙离子依赖的自由基水平有关。
Objective: To investigate the role of trans fatty acids (TFAs) in the process of oxidative low density lipoprotein (LDL) in ECV304 cells and to reveal its mechanism of action. Methods: The expression of HNP-1 in trans fatty acid-stimulated ECV304 cells was detected by real-time fluorescence quantitative PCR. The generation of oxygen free radicals in ECV304 cells and the apoptosis of ECV304 cells were detected by flow cytometry. Lipid oxidation product Malondialdehyde (MDA) production Describes changes in ECL 304 cells’ ability to oxidize LDL. Results: The amount of MDA (nmol / mg) induced by trans-fatty acid was significantly increased (0.155 ± 0.025, P <0.05) and the LDL oxidation was enhanced. The intracellular HNP-1 expression in ECV304 cells stimulated by trans fatty acids (0.429 ± 0.090, P <0.05), while the level of oxygen free radicals increased significantly (66.700 ± 6.532, P <0.05). The use of calcium antagonists could antagonize these effects. CONCLUSION: Trans fatty acids may enhance the ability of ECV304 cells to oxidize LDL by promoting the expression of HNP-1. This increase in oxidative capacity may be related to the level of free radical-dependent calcium ions.