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从M.果实中分离的多糖对HO诱导的RINm5F胰腺β细胞氧化损伤的结构表征及保护作用。

Structural characterization and protective effects of polysaccharides isolated from M. fruits on HO-induced oxidative damage in RINm5F pancreatic β-cells.

作者信息

Lu Xiaohang, Han Lijuan, Deng Yongrong

机构信息

State Key Laboratory of Plateau Ecology and Agriculture, Qinghai University, Xining, China.

College of Agriculture and Animal Husbandry, Qinghai University, Xining, China.

出版信息

Front Nutr. 2025 Aug 6;12:1643051. doi: 10.3389/fnut.2025.1643051. eCollection 2025.

Abstract

Our previous research demonstrated the hypoglycemic and antioxidant properties of crude polysaccharides from M. (BDP), but the structural characteristics and underlying mechanisms were unclear. In this study, a homogeneous polysaccharide, BDP-I, was isolated and structurally characterized. BDP-I had a molecular weight of 3.947 kDa and consisted of arabinose, galactose, glucose, and galacturonic acid, mainly linked through →6)-β-D-GalAp-(1→ glycosidic bonds.An oxidative stress model was established by treating RIN-m5F pancreatic islet cells with 250 μmol/L HO for 3 hours. BDP-I intervention at concentrations ranging from 0.0625 to 0.5 mg/mL significantly improved cell viability, reduced reactive oxygen species (ROS) and thiobarbituric acid reactive substances (TBARS), and enhanced superoxide dismutase (SOD) and catalase (CAT) activities in a dose-dependent manner.Untargeted metabolomics revealed that BDP-I regulated 46 potential biomarkers, effectively reversing metabolic disturbances caused by oxidative stress. In addition, BDP-I modulated the expression of genes associated with apoptosis and mitochondrial damage, including iNOS and NF-κB.These findings suggest that BDP-I exerts protective effects against oxidative damage in pancreatic islet cells through multiple mechanisms, highlighting its potential as a targeted antioxidant agent for functional food or therapeutic applications.

摘要

我们之前的研究证明了来自M.的粗多糖(BDP)的降血糖和抗氧化特性,但结构特征和潜在机制尚不清楚。在本研究中,分离并表征了一种均一多糖BDP-I的结构。BDP-I的分子量为3.947 kDa,由阿拉伯糖、半乳糖、葡萄糖和半乳糖醛酸组成,主要通过→6)-β-D-半乳糖醛酸-(1→糖苷键连接。通过用250μmol/L H₂O₂处理RIN-m5F胰岛细胞3小时建立氧化应激模型。浓度范围为0.0625至0.5 mg/mL的BDP-I干预显著提高了细胞活力,降低了活性氧(ROS)和硫代巴比妥酸反应性物质(TBARS),并以剂量依赖的方式增强了超氧化物歧化酶(SOD)和过氧化氢酶(CAT)的活性。非靶向代谢组学表明,BDP-I调节了46种潜在生物标志物,有效逆转了氧化应激引起的代谢紊乱。此外,BDP-I调节了与细胞凋亡和线粒体损伤相关的基因表达,包括诱导型一氧化氮合酶(iNOS)和核因子κB(NF-κB)。这些发现表明,BDP-I通过多种机制对胰岛细胞氧化损伤发挥保护作用,突出了其作为功能性食品或治疗应用的靶向抗氧化剂的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb45/12364817/ae28a51e03d3/fnut-12-1643051-g001.jpg

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