硫胺素对高糖诱导HT⁃22细胞损伤的神经保护作用  

Neuroprotective Effect of Thiamine on High Glucose‐Induced HT‐22 Cells

作　　者：郭林鑫 赵凡睿 李晏如 刘春雷[1] 吴丹[1] 方丽[1] 闵伟红 GUO Linxin;ZHAO Fanrui;LI Yanru;LIU Chunlei;WU Dan;FANG Li;MIN Weihong(College of Food Science and Engineering,Jilin Agricultural University,Changchun 130118,Jilin,China;College of Food and Health,Zhejiang A&F University,Hangzhou 311300,Zhejiang,China)

机构地区：[1]吉林农业大学食品科学与工程学院,吉林长春130118 [2]浙江农林大学食品与健康学院,浙江杭州311300

出　　处：《食品研究与开发》2025年第6期16-24,共9页Food Research and Development

基　　金：吉林省科技发展计划项目(20210203125SF)。

摘　　要：该研究以高糖诱导HT-22细胞为脑内胰岛素神经元损伤模型,探讨硫胺素对高糖诱导HT-22细胞损伤的神经保护作用。结果表明,硫胺素显著增加细胞内的葡萄糖消耗,表现为葡萄糖摄取荧光探针2-(N-7-硝基-2,1,3-苯并恶二唑-4-氨基)-2-脱氧-D-葡萄糖{2-[N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl)amino]-2-deoxy-D-glucose,2-NBDG}荧光强度和葡萄糖摄取浓度的增加,显著增加高糖诱导下HT-22细胞内胰岛素分泌水平。蛋白免疫印迹试验表明硫胺素显著增加突触相关蛋白表达,调节细胞内β-Catenin/GSK-3β蛋白表达。综上,硫胺素可能通过β-Catenin/GSK-3β信号通路,调节细胞内葡萄糖消耗和摄取,进而增加突触相关蛋白表达,从而改善高糖诱导的神经元损伤。In this work,high glucose-induced HT-22 cells were employed as a model of insulin neuron damage in the brain to evaluate thiamine´s neuroprotective impact on HT-22 cell damage generated by high glucose.The results showed that thiamine significantly increased intracellular glucose consumption,as evidenced by an increase in fluorescence intensity and glucose uptake concentration of the glucose uptake fluorescent probe 2-[N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl)amino]-2-deoxy-D-glucose(2-NBDG),as well as a significant increase in insulin secretion in HT-22 cells induced by high glucose.Western blot tests showed that thiamine dramatically boosted synapse-related protein expression and regulatedβ-Catenin/GSK-3βprotein expression in cells.The above experimental results showed that thiamine may control intracellular glucose consumption and uptake through theβ-Catenin/GSK-3βsignaling pathway,thus boosting the expression of synapse-related proteins and reducing high glucose-induced neuron damage.

关 键 词：硫胺素 高糖损伤 2型糖尿病 HT-22细胞 神经保护 

分 类 号：R73[医药卫生—肿瘤]