Inhibitory actions of selected natural substances on formation of advanced glycation endproducts and advanced oxidation protein products

Abstract

BackgroundAdvanced glycation endproducts (AGE) and advanced oxidation protein products (AOPP) arise as a result of excessive glycation and oxidation processes of proteins in hyperglycemia and oxidative stress conditions respectively, both in vivo and in vitro. In vivo these processes are especially intensified in patients with diabetes, and the adverse effects of AGE and AOPP are particularly unfavorable for the pathogenesis and aggravate the biochemical disturbances and clinical complications of diabetes. Total AGE and AOPP (T-AGE and T-AOPP) are heterogeneous groups of compounds, and they can be divided into two main fractions: high- and low-molecular-weight, i.e. HMW-AGE and HMW-AOPP as well as LMW-AGE and LMW-AOPP. Therefore it is important to find natural substances that will prevent formation of total AGE and AOPP and their high- and low-molecular-weight fractions and thereby reduce their adverse effects on tissues and organs.MethodSelected natural substances and dietary supplements such as vitamin C, aminoguanidine, quercetin and green tea as well as the multicompound formulations Padma Circosan and Padma 28 were tested in an in vitro model using bovine serum albumin (BSA). Fluorescence of T-, HMW- and LMW-AGE and concentration of T-, HMW- and LMW-AOPP were measured after incubation with these substances.ResultsIn the examined concentrations quercetin showed the greatest degree of inhibition for T-AGE (60.5 %) as well as for HMW-AGE (79.5 %), while in the case of LMW-AGE the greatest degree of glycation inhibition was shown by Padma Circosan (74.9 %). T-AOPP and HMW-AOPP were best inhibited by vitamin C (87.3 and 89.1 % respectively). The results obtained for LMW-AOPP are atypical, but the lowest concentration was observed in a sample with Padma 28.ConclusionThe results show that all tested natural compounds have inhibitory activity towards the formation of total and low- and high-molecular-weight forms of AGE and AOPP in vitro. That suggest a possible role in the prevention of diabetic complications, especially the multiherbal compound Padma preparations, which are especially effective in lowering the most dangerous, i.e. LMW fractions.

Static Magnetic Fields Modulate the Response of Different Oxidative Stress Markers in a Restraint Stress Model Animal

“…This was likely due to an increase in the total thiol groups, which decreases oxidative stress and protects the tissues [ 38 , 67 ]. Other studies have also reported similar results [ 65 , 66 ]. We observed that stress increases the lipoperoxidation values, which showed a time-dependent response to SMF exposure.…”

“…Furthermore, AOPPs are proteins (albumin), and their aggregates are often damaged by oxidative stress [ 38 ]. They mostly comprise dityrosines, which allow crosslinking with disulfides through chlorinated oxidants, hypochloric acid, and chloramines, resulting in myeloperoxidase activity [ 65 , 66 ] and the formation of carbonyl groups [ 67 ]. These cause damage to important biological structures, such as proteins, carbohydrates, lipids, and nucleic acids, and may enhance the inflammatory response via NADPH oxidase [ 65 ] or myeloperoxidase action [ 66 ].…”

The Antiglycoxidative Ability of Selected Phenolic Compounds—An In Vitro Study

“…Then chloramine-T (28 mM) was added to all samples and they were incubated for a period of 1 h at 37 °C. Sodium azide (1 mM) as a preservative was used in the experiments [9,86]. Subsequently, all samples were dialyzed and frozen until the time of measurement of glycoxidation products (AOPPs and AGEs).…”

Aminoguanidine reduces diabetes‑associated cardiac fibrosis

“…Here, we propose that AG attenuates the fibrogenic response in T2DM rats, considering that AG reduces AGEs, advanced oxidation protein products (AOPP) (68), and inhibits iNOS activity (69,70), thus reducing oxidative-associated cardiac fibrosis. This was observed in vivo by αSMA IHC, Sirius red/Fast green and Masson's trichrome staining, and confirmed by the in vitro experiments on myofibroblasts.…”

“…Many studies have documented the underlying possible mechanism of AG in diabetes associated cardiac fibrosis, however, the effect of AG on collagen type I deposition through SMAD2/3-ERK1/2 via AGE/RAGE signaling represents the novelty of this study. These can be explained due to the glycation and AOPP-inhibiting properties of AG widely described in the scientific literature (68,71).…”