Abstract
Diabetes mellitus (DM) is a chronic metabolic disease characterized by hyperglycemia. Persistent hyperglycemia causes various complications and vascular damage. Increased production of advanced glycation end products (AGEs) via glycation is involved in DM onset. Previous reports have demonstrated the therapeutic effects of zinc (Zn) complexes on diabetic model mice in vivo. In this study, we aimed to investigate the in vitro anti-glycation effects of the Zn(O4) type Zn complexes, [Zn(mal)2], [Zn(emal)2], [Zn(trp)2], and [Zn(hkt)2]. We determined the effects of the Zn(O4) coordination type complexes on glycation via screening tests of their suppressive effects on fluorescent AGE formation and pentosidine, a fluorescent AGE. The screening test was performed using a phosphate buffer (pH 7.4) at 60°C for 40 h. Then, pentosidine was extracted from the supernatant using MonoSpin AG and quantified using high-performance liquid chromatography-fluorescence analysis. The tested Zn(O4)-type complexes significantly suppressed fluorescent AGE formation more than the positive control, aminoguanidine. Moreover, pentosidine levels were decreased by Zn(O4) complexes with a 7-member troponoide structure, [Zn(trp)2] and [Zn(hkt)2]. To the best of our knowledge, this study is the first to demonstrate the suppressive effects of Zn complexes on glycation reactions in vitro.
