关键词: Blackberry polysaccharides Core-shell structure Glucose/lipid metabolism Nano-selenium particles

Mesh : Humans Selenium / chemistry Hep G2 Cells Polysaccharides / pharmacology chemistry Lipid Metabolism / drug effects Glucose / metabolism Nanoparticles / chemistry Rubus / chemistry Particle Size Oxidative Stress / drug effects Antioxidants / pharmacology Signal Transduction / drug effects

来  源:   DOI:10.1016/j.foodres.2024.114428

Abstract:
In this study, blackberry polysaccharide-selenium nanoparticles (BBP-24-3Se) were first prepared via Na2SeO3/Vc redox reaction, followed by coating with red blood cell membrane (RBC) to form core-shell structure polysaccharide-selenium nanoparticles (RBC@BBP-24-3Se). The particle size of BBP-24-3Se (167.1 nm) was increased to 239.8 nm (RBC@BBP-24-3Se) with an obvious core-shell structure after coating with RBC. FT-IR and XPS results indicated that the interaction between BBP-24-3 and SeNPs formed a new C-O···Se bond with valence state of Se0. Bioassays indicated that RBC coating markedly enhanced both the biocompatibility and bioabsorbability of RBC@BBP-24-3Se, and the absorption rate of RBC@BBP-24-3Se in HepG2 cells was 4.99 times higher than that of BBP-24-3Se at a concentration of 10 μg/mL. Compared with BBP-24-3Se, RBC@BBP-24-3Se possessed significantly heightened protective efficacy against oxidative damage and better regulation of glucose/lipid metabolism disorder induced by palmitic acid in HepG2 cells. Mechanistic studies demonstrated that RBC@BBP-24-3Se could effectively improve PI3K/AKT signaling pathway to promote glucose metabolism, inhibit the expression of lipid synthesis genes and up-regulate the expression of lipid-decomposing genes through AMPK signaling pathway to improve lipid metabolism. These results provided a theoretical basis for developing a new type of selenium supplement for the treatment of insulin resistance.
摘要:
在这项研究中,首先通过Na2SeO3/Vc氧化还原反应制备黑莓多糖-硒纳米颗粒(BBP-24-3Se),然后用红细胞膜(RBC)包被,形成核-壳结构的多糖-硒纳米颗粒(RBC@BBP-24-3Se)。BBP-24-3Se(167.1nm)的粒径增加到239.8nm(RBC@BBP-24-3Se),在用RBC包覆后具有明显的核壳结构。FT-IR和XPS结果表明,BBP-24-3与SeNPs之间的相互作用形成了一个新的C-O··Se键,价态为Se0。生物测定表明,RBC涂层显着增强了RBC@BBP-24-3Se的生物相容性和生物吸收性。浓度为10μg/mL时,RBC@BBP-24-3Se在HepG2细胞中的吸收率是BBP-24-3Se的4.99倍。与BBP-24-3Se相比,RBC@BBP-24-3Se对棕榈酸诱导的HepG2细胞氧化损伤具有明显的保护作用,对糖脂代谢紊乱具有更好的调节作用。机制研究表明,RBC@BBP-24-3Se可有效改善PI3K/AKT信号通路促进糖代谢,抑制脂质合成基因的表达,通过AMPK信号通路上调脂质分解基因的表达,从而改善脂质代谢。这些结果为开发新型补硒治疗胰岛素抵抗提供了理论依据。
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