Abstract As one of the most reactive dicarbonyl compounds, methylglyoxal (MGO) can react with protein to form advanced glycation end products (AGEs), then promoting the development of diabetic complications. Hence, it is significant for preventing protein glycation mediated by MGO. Here, the anti-glycation potential and mechanism of gallocatechin gallate (GCG) as an active ingredient of green tea were investigated. It was found that GCG exhibit good scavenging activities of O2.- and .OH radicals of lysine–MGO system by 92.9% and 15.6%, respectively. The inhibitions (%) of GCG at 354.0 μg/mL for AGEs, dityrosine and N-formylkynurenine in bovine serum albumin (BSA)–MGO system were 96.7%, 97.3% and 98.2%, respectively. GCG (17.8–354.0 μg/mL) trapped MGO in a dose-dependent manner, 82.5% of MGO was trapped and the trapping efficiency reached 46.6% within 12 h when the concentration of GCG was 354.0 μg/mL. Two GCG–mono-MGO adducts were found when the molar ratios of MGO to GCG were 1:3 and 1:6. The efficacy of GCG in recovering the amino groups content, tryptophan residues and hydrophobic pockets of BSA was weak. The binding constant between GCG and BSA was in the order of magnitude of 104 L/mol, and the simulation analysis showed that the GCG–BSA complex was stable. It was inferred that the molecular mechanism of GCG against protein glycation induced by MGO may be due to its scavenging activity of O2.- and .OH radicals, MGO trapping capability and BSA binding interaction. These results suggested that GCG may be a potential inhibitor of MGO-induced glycation and provide new insights into GCG as a dietary supplement in functional foods for ameliorating the diabetic complications of MGO-derived AGEs.

中文翻译：

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没食子儿茶素没食子酸酯影响蛋白质糖化的分子特征

摘要 作为最具活性的二羰基化合物之一，甲基乙二醛（MGO）可与蛋白质反应形成晚期糖基化终末产物（AGEs），进而促进糖尿病并发症的发生。因此，它对于防止由 MGO 介导的蛋白质糖化具有重要意义。在这里，研究了作为绿茶活性成分的没食子儿茶素没食子酸酯 (GCG) 的抗糖化潜力和机制。结果表明，GCG 对赖氨酸-MGO 系统的 O2.- 和 .OH 自由基表现出良好的清除活性，分别为 92.9% 和 15.6%。GCG 在 354.0 μg/mL 时对牛血清白蛋白 (BSA)-MGO 系统中 AGEs、二酪氨酸和 N-甲酰基犬尿氨酸的抑制率 (%) 分别为 96.7%、97.3% 和 98.2%。GCG (17.8–354.0 μg/mL) 以剂量依赖性方式捕获 MGO，捕获了 82.5% 的 MGO，捕获效率达到 46。当 GCG 浓度为 354.0 μg/mL 时，12 h 内为 6%。当 MGO 与 GCG 的摩尔比为 1:3 和 1:6 时，发现了两种 GCG-mono-MGO 加合物。GCG 在恢复 BSA 的氨基含量、色氨酸残基和疏水口袋方面的功效很弱。GCG与BSA的结合常数在104 L/mol的数量级，模拟分析表明GCG-BSA复合物是稳定的。据推测，GCG 对抗 MGO 诱导的蛋白质糖化的分子机制可能是由于其清除 O2.- 和 .OH 自由基的活性、MGO 捕获能力和 BSA 结合相互作用。