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Hydroxy-Selenomethionine, an Organic Selenium Source, Increases Selenoprotein Expression and Positively Modulates the Inflammatory Response of LPS-Stimulated Macrophages
Antioxidants ( IF 6.0 ) Pub Date : 2022-09-22 , DOI: 10.3390/antiox11101876
Joan Campo-Sabariz 1 , Adriana García-Vara 1 , David Moral-Anter 1 , Mickael Briens 2 , Mohammed A Hachemi 2 , Eric Pinloche 2 , Ruth Ferrer 1 , Raquel Martín-Venegas 1
Affiliation  

The role of 2-hydroxy-(4-methylseleno)butanoic acid (OH-SeMet), a form of organic selenium (Se), in selenoprotein synthesis and inflammatory response of THP1-derived macrophages stimulated with lipopolysaccharide (LPS) has been investigated. Glutathione peroxidase (GPX) activity, GPX1 gene expression, selenoprotein P (SELENOP) protein and gene expression, and reactive oxygen species (ROS) production were studied in Se-deprived conditions (6 and 24 h). Then, macrophages were supplemented with OH-SeMet for 72 h and GPX1 and SELENOP gene expression were determined. The protective effect of OH-SeMet against oxidative stress was studied in H2O2-stimulated macrophages, as well as the effect on GPX1 gene expression, oxidative stress, cytokine production (TNFα, IL-1β and IL-10), and phagocytic and killing capacities after LPS stimulation. Se deprivation induced a reduction in GPX activity, GPX1 gene expression, and SELENOP protein and gene expression at 24 h. OH-SeMet upregulated GPX1 and SELENOP gene expression and decreased ROS production after H2O2 treatment. In LPS-stimulated macrophages, OH-SeMet upregulated GPX1 gene expression, enhanced phagocytic and killing capacities, and reduced ROS and cytokine production. Therefore, OH-SeMet supplementation supports selenoprotein expression and controls oxidative burst and cytokine production while enhancing phagocytic and killing capacities, modulating the inflammatory response, and avoiding the potentially toxic insult produced by highly activated macrophages.

中文翻译:

羟基-硒代蛋氨酸是一种有机硒源,可增加硒蛋白的表达并正向调节 LPS 刺激的巨噬细胞的炎症反应

已经研究了 2-羟基-(4-甲基硒) 丁酸 (OH-SeMet)(一种有机硒 (Se))在脂多糖 (LPS) 刺激的 THP1 衍生巨噬细胞的硒蛋白合成和炎症反应中的作用。在缺硒条件下(6 小时和 24 小时)研究了谷胱甘肽过氧化物酶 (GPX) 活性、GPX1 基因表达、硒蛋白 P (SELENOP) 蛋白和基因表达以及活性氧 (ROS) 的产生。然后,用 OH-SeMet 补充巨噬细胞 72 小时,并测定 GPX1 和 SELENOP 基因表达。在H 2 O 2中研究了OH-SeMet对氧化应激的保护作用-刺激的巨噬细胞,以及 LPS 刺激后对 GPX1 基因表达、氧化应激、细胞因子产生(TNFα、IL-1β 和 IL-10)以及吞噬和杀伤能力的影响。硒剥夺导致 24 小时 GPX 活性、GPX1 基因表达以及 SELENOP 蛋白和基因表达降低。OH-SeMet 上调 GPX1 和 SELENOP 基因表达并减少 H 2 O 2后 ROS 的产生治疗。在 LPS 刺激的巨噬细胞中,OH-SeMet 上调 GPX1 基因表达,增强吞噬和杀伤能力,并减少 ROS 和细胞因子的产生。因此,OH-SeMet 补充剂支持硒蛋白表达,控制氧化爆发和细胞因子的产生,同时增强吞噬和杀伤能力,调节炎症反应,避免高度活化的巨噬细胞产生的潜在毒性损伤。
更新日期:2022-09-22
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