色氨酸抑制体外模型中晚期糖基化终末产物形成机理

食源性晚期糖基化终末产物（advanced glycation end products，AGEs）与多种慢性疾病密切相关，尤其是糖尿病和肾脏疾病。为减少AGEs对机体的健康风险，降低食品中AGEs含量，本研究从13?种氨基酸中筛选出具有良好AGEs抑制效果的色氨酸（tryptophan，Trp），利用牛血清白蛋白（bovine serum albumin，BSA）-果糖、BSA-丙酮醛（methylglyoxal，MGO）、BSA-乙二醛（glyoxal，GO）和精氨酸（arginine，Arg）-MGO模型探究Trp对AGEs的抑制机理。结果表明，Trp对荧光AGEs的抑制呈现出显著的质量浓度依赖性。在BSA-GO模型中Trp抑制效果最佳，其次是BSA-MGO模型和Arg-MGO模型，而在BSA-果糖模型中抑制效果不明显。Trp对Nε-羧甲基赖氨酸（Nε-carboxymethyllysine，CML）和Nε-羧乙基赖氨酸（Nε-carboxyethyllysine，CEL）的抑制呈现钟形曲线，在1 000 μg/mL下对CML和CEL的抑制率最高。通过探究Trp捕获MGO的能力发现，其可通过芳香亲电子取代和Pictet-Spengler反应捕获MGO，最高捕获能力为3 mol。

Inhibitory Mechanism of Tryptophan on the Formation of Advanced Glycation End Products in Vitro

The intake of dietary advanced glycation end products (AGEs) is closely related to a variety of chronic diseases, especially diabetes and kidney disease. In this study, 13 amino acids were screened for their inhibitory activity on AGEs, revealing that tryptophan (Trp) was selected to evaluate its mechanism of action against the formation of AGEs in bovine serum albumin (BSA)-fructose, BSA-methylglyoxal (MGO), BSA-glyoxal (GO) and arginine (Arg)-MGO models. The inhibitory effect of Trp on fluorescent AGEs was concentration dependent. In BSA-MGO model, the inhibitory effect of Trp on the formation of AGEs was the best, followed by BSA-GO and Arg-MGO models, and Trp had little effect on BSA-fructose mode. The inhibition of different concentrations of Trp on Nε-carboxymethyl lysine (CML) and Nε-carboxyethyl lysine (CEL) showed a bell-shaped curve with the highest inhibition efficiency being observed at 1 000 μg/mL concentration. Moreover, it was found that Trp could capture MGO by aromatic electron affinity substitution and the Pictet Spengler reaction, with a maximum trapping capacity of 3 molars.