Antiglycation Activity of Aucubin In Vitro and in Exogenous Methylglyoxal Injected Rats

Abstract

Advanced glycation end products (AGEs) is a causative factor of various chronic diseases, including chronic kidney disease and atherosclerosis. AGE inhibitors, such as aminoguanidine and pyridoxamine, have the therapeutic activities for reversing the increase in AGEs burden. This study evaluated the inhibitory effects of aucubin on the formation of methylglyoxal (MGO)-modified AGEs in vitro. We also determined the potential activity of aucubin in reducing the AGEs burden in the kidney, blood vessel, heart, and retina of exogenously MGO-injected rats. Aucubin inhibited the formation of MGO-modified AGE-bovine serum albumin (IC50 = 0.57 ± 0.04 mmol/L) and its cross-links to collagen (IC50 = 0.55 ± 0.02 mmol/L) in a dose-dependent manner. In addition, aucubin directly trapped MGO (IC50 = 0.22 ± 0.01 mmol/L) in vitro. In exogenous MGO-injected rats, aucubin suppressed the formation of circulating AGEs and its accumulation in various tissues. These activities of aucubin on the MGO-derived AGEs in vitro and in vivo showed its pharmacological potential for inhibiting AGEs-related various chronic diseases.

Df-5 Compound Delays Development of Diabetic Nephropathy in Rats

“…Согласно первоначальным предположениям, выдвинутым для аналога соединения ALT-711 -фенилтиазолия бромида [16], механизм его действия включает разрыв С-С связи между двумя соседними карбонильными группами. Однако КПГ, содержащие подобный 1,2-дикарбонильный фрагмент, в условиях эксперимента установлены не были, хотя разрыв поперечных сшивок был доказан экспериментально, иммунологически, с применением антител к тому или иному из двух сшитых белков [30][31][32][33]. Следует отметить, что такая С-С связь, расположенная между двумя соседними карбонильными группами, присутствует в некоторых ранних продуктах гликирования [22].…”

Characteristics, Isolation Methods, and Biological Properties of Aucubin

“…Examining the antiglycation activity in vitro at concentrations of 0.22 mmol/L and in vivo at 10 and 25 mg/kg revealed that aucubin suppressed the formation of advanced glycation end products (AGEs). This inhibitory effect on the formation of AGEs is dose-dependent [ 79 ]. AGEs are a causative factor for, among others, chronic kidney disease and atherosclerosis.…”

“…In another work, administering oral aucubin at a dose of 15 mg/kg BW prevented retinal degeneration induced using N-methyl-N-nitrosourea in mice. This effect is believed to result from the inhibition of oxidative damage and apoptosis of DNA, as shown by the decrease in 8-OHdG generally formed due to the generation of excess ROS [ 79 ].…”