Lu Xiaohang, Han Lijuan, Deng Yongrong
State Key Laboratory of Plateau Ecology and Agriculture, Qinghai University, Xining, China.
College of Agriculture and Animal Husbandry, Qinghai University, Xining, China.
Front Nutr. 2025 Aug 6;12:1643051. doi: 10.3389/fnut.2025.1643051. eCollection 2025.
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.
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。
