食品科学 ›› 2025, Vol. 46 ›› Issue (5): 161-169.doi: 10.7506/spkx1002-6630-20240424-225

• 营养卫生 • 上一篇    下一篇

原花青素B2对高糖诱导SH-SY5Y细胞铁死亡的抑制作用及机制

王佳琪,陈秀婷,夏星,周金玲   

  1. (1.广西中医药大学药学院,广西 南宁 530200;2.广西中医药大学 广西高校中药神经-代谢及免疫药理重点实验室,广西 南宁 530200)
  • 出版日期:2025-03-15 发布日期:2025-02-07
  • 基金资助:
    国家自然科学基金地区科学基金项目(81960728);广西高校中青年教师科研基础能力提升项目(2022KY0302); 广西中医药大学2021年博士科研启动基金项目(2021BS007);广西中医药大学桂派杏林拔尖人才项目(2022C007); 广西中医药大学桂派中医药传承创新团队项目(2022B005); 广西高水平中医药重点学科中药药理学项目(桂中医药科教发〔2023〕13号); 广西中医药大学岐黄工程高层次人才团队培育项目(202405)

Inhibitory Effect and Mechanism of Procyanidin B2 on High Glucose-Induced Ferroptosis in SH-SY5Y Cells

WANG Jiaqi, CHEN Xiuting, XIA Xing, ZHOU Jinling   

  1. (1. School of Pharmacy, Guangxi University of Chinese Medicine, Nanning 530200, China; 2. Key Laboratory of TCM Neuro-metabolism and Immunopharmacology of Guangxi Education Department, Guangxi University of Chinese Medicine, Nanning 530200, China)
  • Online:2025-03-15 Published:2025-02-07

摘要: 目的:研究原花青素B2对高糖诱导人神经母细胞瘤(SH-SY5Y)分化细胞铁死亡的神经保护作用及相关机制。方法:以45 mmol/L的葡萄糖处理分化后的SH-SY5Y细胞构建高糖诱导体外损伤细胞模型。随机分为正常对照组、高糖模型组、高质量浓度原花青素B2治疗组、低质量浓度原花青素B2治疗组、利普司他汀-1(阳性对照)组。采用CCK8法检测细胞活力,流式细胞术检测Fe2+和脂质过氧化物(lipid peroxide,LPO)水平,免疫荧光法检测脂质活性氧(reactive oxygen species,ROS)水平,JC-1染色法检测细胞线粒体膜电位,透射电镜观察细胞线粒体铁死亡特征性形态变化,利用Western blot法检测铁死亡相关蛋白溶质载体家族7成员11(solute carrier family 7 member 11,SLC7A11)和转铁蛋白受体(transferrin receptor,TFRC)水平变化。结果:与正常对照组比较,高糖模型组的细胞活力、细胞线粒体膜电位、还原型谷胱甘肽(reduced glutathione,GSH)/氧化型谷胱甘肽(oxidized glutathione,GSSG)比值以及SLC7A11蛋白表达水平显著下降,细胞内Fe2+、LPO、脂质ROS和TFRC蛋白水平显著上升。与高糖模型组比较,一定质量浓度的原花青素B2能够明显上调细胞活力、细胞线粒体膜电位、GSH/GSSG比值以及SLC7A11蛋白表达水平,同时下调LPO、脂质ROS水平。透射电镜观察结果显示原花青素B2明显改善了高糖引起的细胞线粒体萎缩、脊断裂、消失等畸变现象。结论:原花青素B2能抑制高糖诱导SH-SY5Y分化细胞的脂质过氧化损伤,其作用机制与其通过调节谷胱甘肽途径抑制铁死亡有关。

关键词: 原花青素B2;高糖损伤;铁死亡;SH-SY5Y细胞;神经保护

Abstract: Objective: To investigate the neuroprotective effect and mechanism of procyanidin B2 on high glucose-induced ferroptosis in differentiated SH-SY5Y cells. Methods: An in vitro cell injury model was created by treating differentiated SH-SY5Y cells with 45 mmol/L glucose, and the cells were randomly divided into normal control, high-glucose model, high-concentration procyanidin B2 treatment, low-concentration procyanidin B2 treatment, and positive control drug lipvastatin-1 groups. The CCK8 method was used to observe cell viability. Flow cytometry was used to detect Fe2+ and lipid peroxide (LPO) levels, immunofluorescence was used to detect lipid reactive oxygen species (ROS) levels, JC-1 staining was used to detect mitochondrial membrane potential, transmission electron microscopy (TEM) was used to observe morphological changes characteristic of mitochondrial ferroptosis, and Western blot was used to detect the expression levels of ferroptosis-related proteins including solute carrier family 7 member 11 (SLC7A11) and transferrin receptor (TFRC). Results: Compared with the normal control group, the high glucose model group showed a significant decrease in cell viability and mitochondrial membrane potential, reduced glutathione (GSH)/oxidized glutathione (GSSG) ratio, and SLC7A11 protein expression level, while the intracellular levels of Fe2+, LPO, lipid ROS, and TFRC increased obviously. Compared with the high glucose group, a certain concentration of procyanidin B2 significantly increased cell viability, mitochondrial membrane potential, GSH/GSSG ratio, and SLC7A11 protein expression and simultaneously down-regulated LPO and lipid ROS levels. The TEM results showed that procyanidin B2 significantly alleviated mitochondrial shrinkage, cristae rupture and disappearance, and other distortions caused by high glucose. Conclusion: Procyanidin B2 can inhibit lipid peroxidation damage induced by high glucose in differentiated SH-SY5Y cells, and its action mechanism is related to the inhibition of ferroptosis by regulating the glutathione pathway.

Key words: procyanidin B2; high glucose-induced damage; ferroptosis; SH-SY5Y cells; neuroprotection

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