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用玫瑰果多糖对硒纳米粒子进行生物功能化及其对 HO 诱导的 INS-1 细胞凋亡的保护作用。

Biofunctionalization of selenium nanoparticles with a polysaccharide from Rosa roxburghii fruit and their protective effect against HO-induced apoptosis in INS-1 cells.

机构信息

School of Food Science and Engineering, Guangdong Province Key Laboratory for Green Processing of Natural Products and Product Safety, South China University of Technology, Guangzhou 510640, China.

出版信息

Food Funct. 2019 Feb 20;10(2):539-553. doi: 10.1039/c8fo01958d.

DOI:10.1039/c8fo01958d
PMID:30662993
Abstract

Defective glucose-stimulated insulin secretion (GSIS) induced by chronic exposure to reactive oxygen species (ROS) is a hallmark of type 2 diabetes mellitus (T2DM). Therefore, it is of great interest to search for biofunctional agents with antioxidant activity to protect pancreatic islet cells from oxidative damage. In the present study, selenium nanoparticles (SeNPs) functionalized with a novel polysaccharide (RTFP-3) extracted from Rosa roxburghii fruit were first prepared via a facile, single-step and green in situ synthesis method. The in vitro protective effects of RP3-SeNPs on INS-1 cells against H2O2-induced cell apoptosis were investigated. Structural characterization indicated that RTFP-3-functionalized SeNPs (RP3-SeNPs) with an average diameter of 104.5 nm were highly uniform and extremely stable in comparison with bare SeNPs. The results of bioassays revealed that RP3-SeNPs possessed much higher protective and suppressive activities against H2O2-induced apoptosis of INS-1 cells in comparison with their individual components. After treatment with an RP3-SeNPs solution (2 μg mL-1), the cell viability of INS-1 cells reached about 89.34%. Mechanistic studies demonstrated that RP3-SeNPs effectively blocked the overproduction of intracellular ROS, mitochondrial damage, and the activation of caspase-3, caspase-8, and caspase-9 in INS-1 cells, which indicated that RP3-SeNPs functioned via attenuating oxidative stress and downregulating the expression of uncoupling protein-2 (UCP-2). Our findings suggest that RP3-SeNPs can function as a promising candidate to prevent or limit the dysfunction of β-cells.

摘要

慢性暴露于活性氧(ROS)导致的葡萄糖刺激胰岛素分泌(GSIS)缺陷是 2 型糖尿病(T2DM)的一个标志。因此,寻找具有抗氧化活性的生物功能制剂来保护胰岛细胞免受氧化损伤具有重要意义。在本研究中,首次通过简便、单步和绿色的原位合成方法,用从玫瑰果实中提取的新型多糖(RTFP-3)对硒纳米粒子(SeNPs)进行了功能化。研究了 RTFP-3-SeNPs 对 H2O2 诱导的 INS-1 细胞凋亡的体外保护作用。结构表征表明,与裸 SeNPs 相比,RTFP-3 功能化的 SeNPs(RP3-SeNPs)具有更高的均匀性和稳定性,平均粒径为 104.5nm。生物测定结果表明,与它们的各个组成部分相比,RP3-SeNPs 对 H2O2 诱导的 INS-1 细胞凋亡具有更高的保护和抑制作用。用 RP3-SeNPs 溶液(2μg mL-1)处理后,INS-1 细胞的细胞活力达到约 89.34%。机制研究表明,RP3-SeNPs 能有效阻断 INS-1 细胞内 ROS 的过度产生、线粒体损伤以及 caspase-3、caspase-8 和 caspase-9 的激活,这表明 RP3-SeNPs 通过减轻氧化应激和下调解偶联蛋白-2(UCP-2)的表达来发挥作用。我们的研究结果表明,RP3-SeNPs 可以作为一种有前途的候选药物,用于预防或限制β细胞的功能障碍。

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