Pap Ramóna, Pandur Edina, Jánosa Gergely, Sipos Katalin, Agócs Attila, Deli József
Department of Pharmaceutical Biology, Faculty of Pharmacy, University of Pécs, Rókus u. 2., H-7624 Pécs, Hungary.
Department of Biochemistry and Medical Chemistry, Medical School, University of Pécs, Szigeti út 12., H-7624 Pécs, Hungary.
Antioxidants (Basel). 2021 Feb 27;10(3):363. doi: 10.3390/antiox10030363.
Lutein is a tetraterpene carotenoid, which has been reported as an important antioxidant and it is widely used as a supplement. Oxidative stress participates in many human diseases, including different types of neurodegenerative disorders. Microglia, the primary immune effector cells in the central nervous system, are implicated in these disorders by producing harmful substances such as reactive oxygen species (ROS). The protective mechanisms which scavenge ROS include enzymes and antioxidant substances. The protective effects of different carotenoids against oxidative stress have been described previously. Our study focuses on the effects of lutein on antioxidant enzymes, cytokines and iron metabolism under stress conditions in BV-2 microglia. We performed cell culture experiments: BV-2 cells were treated with lutein and/or with HO; the latter was used for inducing oxidative stress in microglial cells. Real-time PCR was performed for gene expression analyses of antioxidant enzymes, and ELISA was used for the detection of pro- and anti-inflammatory cytokines. Our results show that the application of lutein suppressed the HO-induced ROS (10': 7.5 ng + 10 µM HO = 0.0002; 10 ng/µL + 10 µM HO = 0.0007), influenced iron utilization and changed the anti-inflammatory and pro-inflammatory cytokine secretions in BV-2 cells. Lutein increased the IL-10 secretions compared to control (24 h: 7.5 ng/µL = 0.0274; 10 ng/µL = 0.0008) and to 10 µM HO-treated cells (24 h: 7.5 ng/µL + HO = 0.0003; 10 ng/µL + HO = 0.0003), while it decreased the TNFα secretions compared to HO treated cells (24 h: 7.5 ng/µL + HO < 0.0001; 10 ng/µL + HO < 0.0001). These results contribute to understanding the effects of lutein, which may help in preventing or suppressing ROS-mediated microglia activation, which is related to neuronal degeneration in oxidative stress scenario.
叶黄素是一种四萜类胡萝卜素，据报道它是一种重要的抗氧化剂，并且被广泛用作补充剂。氧化应激参与许多人类疾病，包括不同类型的神经退行性疾病。小胶质细胞是中枢神经系统中的主要免疫效应细胞，通过产生诸如活性氧（ROS）等有害物质而与这些疾病有关。清除ROS的保护机制包括酶和抗氧化物质。先前已经描述了不同类胡萝卜素对氧化应激的保护作用。我们的研究重点是叶黄素在应激条件下对BV-2小胶质细胞中抗氧化酶、细胞因子和铁代谢的影响。我们进行了细胞培养实验：用叶黄素和/或HO处理BV-2细胞；后者用于在小胶质细胞中诱导氧化应激。通过实时PCR进行抗氧化酶的基因表达分析，并使用ELISA检测促炎和抗炎细胞因子。我们的结果表明，叶黄素的应用抑制了HO诱导的ROS（10': 7.5 ng + 10 µM HO = 0.0002；10 ng/µL + 10 µM HO = 0.0007），影响了铁的利用，并改变了BV-2细胞中抗炎和促炎细胞因子的分泌。与对照相比（24小时：7.5 ng/µL = 0.0274；10 ng/µL = 0.0008）以及与10 µM HO处理的细胞相比（24小时：7.5 ng/µL + HO = 0.0003；10 ng/µL + HO = 0.0003），叶黄素增加了IL-10的分泌，而与HO处理的细胞相比（24小时：7.5 ng/µL + HO < 0.0001；10 ng/µL + HO < 0.0001），它降低了TNFα的分泌。这些结果有助于理解叶黄素可能有助于预防或抑制ROS介导的小胶质细胞激活的作用，这与氧化应激情况下的神经元变性有关。
