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目的:探讨反式脂肪酸(TFAs)对ECV304细胞氧化低密度脂蛋白(ox-LDL)的作用及其机制。方法:按常规方法传代培养ECV304细胞,用实时荧光定量PCR检测不同浓度TEAs刺激(TFA处理组)后ECV304细胞中HNP-1的表达;采用流式细胞仪检测ECV304细胞中氧自由基(ROS)的生成;用脂质氧化产物丙二醛(MDA)生成量描述ECV304细胞LDL氧化能力的变化。并与未行TFAs处理的ECV304细胞对照组比较其组间差异。结果:与对照组比较,TFAS处理组HNP-1mRNA表达水平显著升高(0.220±0.030vs 0.429±0.090,P<0.05);与对照组比较,1mmol/L TFAS刺激ECV304细胞12h其ROS水平显著升高(11.30±1.67vs 66.70±6.53,P<0.05),在加入不同钙离子拮抗剂后ROS水平明显下降(P<0.05);与LDL处理组比较,1mmol/L TFAS+LDL处理组MDA水平也显著升高(0.134±0.027vs 0.155±0.025,P<0.05)。结论:反式脂肪酸能促进HNP-1的表达,提高钙离子依赖的自由基水平,从而提高ECV304细胞氧化LDL的能力。
Objective: To investigate the effect and mechanism of trans fatty acids (TFAs) on ox-LDL in ECV304 cells. Methods: The ECV304 cells were subcultured by conventional methods and the expression of HNP-1 in ECV304 cells was detected by real-time fluorescence quantitative PCR. The expressions of oxygen free radicals (ROS) in ECV304 cells were detected by flow cytometry The production of MDA was used to describe the changes of LDL oxidation in ECV304 cells. The difference between groups was compared with that of ECV304 cells without TFAs treatment. Results: Compared with the control group, the expression level of HNP-1 mRNA in TFAS group was significantly increased (0.220 ± 0.030 vs 0.429 ± 0.090, P <0.05). Compared with the control group, the ROS level was significantly increased at 1 mmol / L TFAS stimulation of ECV304 cells (11.30 ± 1.67 vs 66.70 ± 6.53, P <0.05). The levels of ROS decreased significantly (P <0.05) after adding different calcium channel blockers. Compared with LDL group, MDA level in TFAR + LDL group (0.134 ± 0.027 vs 0.155 ± 0.025, P <0.05). CONCLUSION: Trans fatty acids can promote the expression of HNP-1 and increase the level of free radical-dependent calcium ions, thereby enhancing the ability of ECV304 cells to oxidize LDL.