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首页> 外文期刊>Balkan Medical Journal >Caffeine Increases Apolipoprotein A-1 and Paraoxonase-1 but not Paraoxonase-3 Protein Levels in Human-Derived Liver (HepG2) Cells
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Caffeine Increases Apolipoprotein A-1 and Paraoxonase-1 but not Paraoxonase-3 Protein Levels in Human-Derived Liver (HepG2) Cells

机译:咖啡因增加人源性肝(HepG2)细胞中载脂蛋白A-1和对氧磷酶-1,但不使对氧磷酶-3蛋白水平升高。

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Background: Apolipoprotein A-1, paraoxonase-1 and paraoxonase-3 are antioxidant and anti-atherosclerotic structural high-density lipoprotein proteins that are mainly synthesized by the liver. No study has ever been performed to specifically examine the effects of caffeine on paraoxonase enzymes and on liver apolipoprotein A-1 protein levels. Aims: To investigate the dose-dependent effects of caffeine on liver apolipoprotein A-1, paraoxonase-1 and paraoxonase-3 protein levels. Study Design: In vitro experimental study. Methods: HepG2 cells were incubated with 0 (control), 10, 50 and 200 μM of caffeine for 24 hours. Cell viability was evaluated by 3-(4,5-Dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide assay. Apolipoprotein A-1, paraoxonase-1 and paraoxonase-3 protein levels were measured by western blotting. Results: We observed a significant increase on apolipoprotein A-1 and paraoxonase-1 protein levels in the cells incubated with 50 μM of caffeine and a significant increase on paraoxonase-1 protein level in the cells incubated with 200 μM of caffeine. Conclusion: Our study showed that caffeine does not change paraoxonase-3 protein level, but the higher doses used in our study do cause an increase in both apolipoprotein A-1 and paraoxonase-1 protein levels in liver cells.
机译:背景:载脂蛋白A-1,对氧磷酶-1和对氧磷酶-3是抗氧化剂和抗动脉粥样硬化结构的高密度脂蛋白,主要由肝脏合成。尚未进行过专门研究咖啡因对对氧磷酶和肝载脂蛋白A-1蛋白水平影响的研究。目的:研究咖啡因对肝载脂蛋白A-1,对氧磷酶-1和对氧磷酶-3蛋白水平的剂量依赖性作用。研究设计:体外实验研究。方法:将HepG2细胞与0(对照),10、50和200μM咖啡因孵育24小时。细胞存活力通过3-(4,5-二甲基-2-噻唑基)-2,5-二苯基-2H-溴化四唑测定来评估。通过蛋白质印迹法测定载脂蛋白A-1,对氧磷酶-1和对氧磷酶-3的蛋白水平。结果:我们观察到与50μM咖啡因孵育的细胞中载脂蛋白A-1和对氧磷酶1蛋白水平显着增加,与200μM咖啡因孵育的细胞中对氧磷酶1蛋白水平显着增加。结论:我们的研究表明咖啡因不会改变对氧磷酶3蛋白的水平,但是我们研究中使用的较高剂量确实会引起肝细胞载脂蛋白A-1和对氧磷酶1蛋白水平的增加。

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