Department of Life Sciences , University of Modena and Reggio Emilia , Via Amendola 2 , 42100 Reggio Emilia , Italy.
J Agric Food Chem. 2019 Jul 17;67(28):7821-7831. doi: 10.1021/acs.jafc.9b02357. Epub 2019 Jul 9.
The mechanism of inhibition of advanced glycation end product (AGE) formation by protocatechuic acid and 3,4-dihydroxyphenylacetic acid (DHPA) has been studied using a widespread applied model system composed of bovine serum albumin (BSA) and supraphysiological glucose concentrations. Protocatechuic acid and DHPA inhibited the formation of Amadori compounds, fluorescent AGEs (IC = 62.1 ± 1.4 and 155.4 ± 1.1 μmol/L, respectively), and -(carboxymethyl)lysine (IC = 535.3 ± 1.1 and 751.2 ± 1.0 μmol/L, respectively). BSA was pretreated with the two phenolic acids, and the formation of BSA-phenolic acid adducts was estimated by nanoflow liquid chromatography-electrospray ionization-quadrupole time-of-flight mass spectrometry. Results showed that the tested phenolic acids bound key sites of glycation in BSA through a metal-catalyzed oxidative mechanism. The antiglycative activity mechanism involved the formation of BSA-phenolic acid adducts, and it is unlikely that this occurs . These results raise the problem to design models closer to physiological conditions to reach biologically sound conclusions.
已采用广泛应用的模型系统（由牛血清白蛋白（BSA）和超生理浓度的葡萄糖组成）研究了原儿茶酸和 3,4-二羟基苯乙酸（DHPA）抑制晚期糖基化终产物（AGE）形成的机制。原儿茶酸和 DHPA 抑制了 Amadori 化合物、荧光 AGE（IC = 62.1 ± 1.4 和 155.4 ± 1.1 μmol/L）和 -(羧甲基)赖氨酸（IC = 535.3 ± 1.1 和 751.2 ± 1.0 μmol/L）的形成。用两种酚酸预处理 BSA，通过纳流液相色谱-电喷雾电离-四极杆飞行时间质谱法估算 BSA-酚酸加合物的形成。结果表明，测试的酚酸通过金属催化氧化机制结合 BSA 中糖基化的关键部位。抗糖化活性机制涉及 BSA-酚酸加合物的形成，而且不太可能发生这种情况。这些结果提出了设计更接近生理条件的模型以得出合理生物学结论的问题。
