Inhibition of advanced glycation end products by red grape skin extract and its antioxidant activity

Abstract

BackgroundThe objective of the present study was to determine the phytochemical content and the protective effect of red grape skin extract (RGSE) against fructose-mediated protein oxidation. In addition, RGSE was screened for its potential as an antioxidant using various in vitro models.MethodsAntioxidant activity was measured by 2,2-diphenyl-1-picrylhydrazyl (DPPH), hydroxyl radical scavenging activity, superoxide radical scavenging activity, trolox equivalent antioxidant capacity, ferric reducing antioxidant power (FRAP), ferrous ion chelating power. The total phenols content was measured by Folin–Ciocalteu assay, the flavonoids content by the AlCl3 colorimetric method. Antiglycation activity was determined using the formation of AGE fluorescence intensity, Nϵ-(carboxymethyl)lysine, and the level of fructosamine. The protein oxidation was examined using the level of protein carbonyl content and thiol group.ResultsThe results showed that the content of total phenolics, flavonoids and total anthocyanins in RGSE was 246.3 ± 0.9 mg gallic acid equivalent/g dried extract, 215.9 ± 1.3 mg catechin equivalent/g dried extract, and 36.7 ± 0.8 mg cyanidin-3-glucoside equivalent/g dried extract, respectively. In the DPPH radical scavenging activity, hydroxyl radical scavenging activity, and superoxide radical scavenging activity, RGSE had the IC50 values of 0.03 ± 0.01 mg/ml, 5.40 ± 0.01 mg/ml, and 0.58 ± 0.01 mg/ml, respectively. In addition, RGSE had trolox equivalent antioxidant capacity assay (395.65 ± 1.61 mg trolox equivalent/g dried extract), ferric reducing antioxidant power (114.24 ± 0.03 mM FeSO4/g dried extract), and ferrous ion chelating power (3,474.05 ± 5.55 mg EDTA/g dried extract), respectively. The results showed that RGSE at different concentrations (0.031–0.500 mg/ml) has significantly inhibited the formation of AGEs in terms of the fluorescence intensity of glycated BSA during 4 weeks of study. The RGSE markedly decreased the level of fructosamine, which is directly associated with the reduction of AGE formation and Nϵ-(carboxymethyl)lysine (CML). The results demonstrated the significant effect of RGSE on preventing protein oxidative damages, including effects on the thiol and protein carbonyl oxidation.ConclusionsThe present study revealed that RGSE would exert beneficial effects by virtue of its antioxidants and antiglycation. The findings could provide a new insight into the naturally occurring antiglycation properties of RGSE for preventing AGE-mediated diabetic complication.

Protective effects of cyanidin-3-rutinoside against monosaccharides-induced protein glycation and oxidation

“…Recent data indicate that anthocyanin-enriched red grape skin extract demonstrates the ability to reduce the formation of AGEs, glycation-induced protein oxidation in BSA [35]. In the present study, we firstly investigated the effect of C3R on different types of monosaccharideinduced protein glycation.…”

Protein glycation inhibitory activity and antioxidant capacity of clove extract

“…Several edible plants including berries (Wang et al 2011), red grape skin (Jariyapamornkoon et al 2013), pomelo (Caengprasath et al 2013), and Cyperus rotundus (Ardestani and Yazdanparast 2007), have shown antiglycation activities in BSA-fructose models. The major components of edible plants contain high phenolic compounds and flavonoids such as catechin, epicatechin, quercetin, rutin, kaempferol, p r o a n t h o c y a n i d i n s , h e s p e r i d i n , n e o h e s p e r i d i n dihydrochalcone, ellagic acid, gallic acid, and p-coumaric acid.…”

Inhibition of Advanced Glycation End-Product Formation by Quercetin and Catechin: An Alternative Therapy for Treating Diabetic Complications

“…Eugenol, a phenylpropanoid from Ocimum Gratissimum, is an FDAapproved inhibitor of AGE that can be used for the management of diabetes and complications [25]. Compounds with AGE inhibiting property also act as natural ROS scavengers [26,27]. Polyol pathwayinduced AGE formation might be controlled by inhibiting the activity of ALR2.…”