Peng Xi, Hu Xing, Liu Kai, Gong Deming, Zhang Guowen
State Key Laboratory of Food Science and Technology, Nanchang University, Nanchang 330047, China; Jiangxi Biotech Vocational College, Nanchang 330200, China.
State Key Laboratory of Food Science and Technology, Nanchang University, Nanchang 330047, China.
Food Chem. 2023 Aug 1;416:135801. doi: 10.1016/j.foodchem.2023.135801. Epub 2023 Feb 28.
Inhibition of advanced glycation end products (AGEs) formed in protein glycosylation is crucial for minimizing diabetic complications. Herein, the anti-glycation potential of hesperetin-Cu (II) complex was investigated. Hesperetin-Cu (II) complex strongly inhibited three stages glycosylation products in bovine serum albumin (BSA)-fructose model, especially for the inhibition of AGEs (88.45%), which was stronger than hesperetin (51.76%) and aminoguanidine (22.89%). Meanwhile, hesperetin-Cu (II) complex decreased the levels of BSA carbonylation and oxidation products. 182.50 µg/mL of hesperetin-Cu (II) complex inhibited 66.71% β-crosslinking structures of BSA, and scavenged 59.80% superoxide anions and 79.76% hydroxyl radicals. Moreover, after incubating with methylglyoxal for 24 h, hesperetin-Cu (II) complex removed 85.70% methylglyoxal. The mechanisms of protein antiglycation by hesperetin-Cu (II) complex may be through protecting structure, trapping methylglyoxal, scavenging free radicals and interacting with BSA. This study may contribute to the development of hesperetin-Cu (II) complex as a functional food additive against protein glycation.
抑制蛋白质糖基化过程中形成的晚期糖基化终产物（AGEs）对于将糖尿病并发症降至最低至关重要。在此，研究了橙皮素 - 铜（II）配合物的抗糖基化潜力。橙皮素 - 铜（II）配合物在牛血清白蛋白（BSA） - 果糖模型中强烈抑制糖基化的三个阶段产物，特别是对AGEs的抑制（88.45%），其抑制作用强于橙皮素（51.76%）和氨基胍（22.89%）。同时，橙皮素 - 铜（II）配合物降低了BSA羰基化和氧化产物的水平。182.50 µg/mL的橙皮素 - 铜（II）配合物抑制了66.71%的BSA β - 交联结构，并清除了59.80%的超氧阴离子和79.76%的羟基自由基。此外，与甲基乙二醛孵育24小时后，橙皮素 - 铜（II）配合物去除了85.70%的甲基乙二醛。橙皮素 - 铜（II）配合物的蛋白质抗糖基化机制可能是通过保护结构、捕获甲基乙二醛、清除自由基以及与BSA相互作用。本研究可能有助于将橙皮素 - 铜（II）配合物开发为一种抗蛋白质糖基化的功能性食品添加剂。
