Departamento de Metabolismo y Nutrición; Instituto de Ciencia y Tecnología de Alimentos y Nutrición (ICTAN - CSIC), Madrid, Spain; Centro de Investigación Biomédica en red de Diabetes y Enfermedades Metabólicas Asociadas (ISCIII), Madrid, Spain.
Mol Nutr Food Res. 2014 Mar;58(3):447-56. doi: 10.1002/mnfr.201300291. Epub 2013 Oct 1.
Diabetes mellitus is associated with reductions in glutathione, supporting the critical role of oxidative stress in its pathogenesis. Antioxidant food components such as flavonoids have a protective role against oxidative stress-induced degenerative and age-related diseases. Flavonoids such as epicatechin (EC) constitute an important part of the human diet; they can be found in green tea, grapes, and cocoa and possess multiple biological activities. This study investigates the chemo-protective effect of EC against oxidative stress induced by tert-butylhydroperoxide (t-BOOH) on Ins-1E pancreatic beta cells.
Cell viability, oxidative status, phosphorylated Jun kinase (p-JNK) expression, and insulin secretion were evaluated. Ins-1E cells treatment with 5-20 μM EC for 20 h evoked no cell damage and enhanced antioxidant enzymes and insulin secretion. Addition of 50 μM t-BOOH for 2 h induced reactive oxygen species, p-JNK, and carbonyl groups and decreased GSH and insulin secretion. Pretreatment of cells with EC prevented the t-BOOH-induced reactive oxygen species, carbonyl groups, p-JNK expression and cell death, and recovered insulin secretion.
Ins-1E cells treated with EC showed a remarkable recovery of cell viability and insulin secretion damaged by t-BOOH, indicating that integrity of secreting and surviving machineries in the EC-treated cells was notably protected against the oxidative insult.
糖尿病与谷胱甘肽减少有关，这支持了氧化应激在其发病机制中的关键作用。抗氧化食品成分，如类黄酮，对氧化应激诱导的退行性和与年龄相关的疾病具有保护作用。类黄酮，如表儿茶素（EC），构成了人类饮食的重要组成部分；它们存在于绿茶、葡萄和可可中，具有多种生物活性。本研究调查了 EC 对胰岛β细胞 Ins-1E 中由叔丁基过氧化物（t-BOOH）诱导的氧化应激的化学保护作用。
评估了细胞活力、氧化状态、磷酸化 Jun 激酶（p-JNK）表达和胰岛素分泌。Ins-1E 细胞用 5-20 μM EC 处理 20 h 不会引起细胞损伤，并增强抗氧化酶和胰岛素分泌。用 50 μM t-BOOH 处理 2 h 诱导活性氧、p-JNK 和羰基，并降低 GSH 和胰岛素分泌。用 EC 预处理细胞可防止 t-BOOH 诱导的活性氧、羰基、p-JNK 表达和细胞死亡，并恢复胰岛素分泌。
用 EC 处理的 Ins-1E 细胞显示出对 t-BOOH 损伤的细胞活力和胰岛素分泌的显著恢复，表明 EC 处理的细胞中分泌和存活机制的完整性明显受到氧化应激的保护。
