Moringa oleifera aqueous leaf extract inhibits reducing monosaccharide-induced protein glycation and oxidation of bovine serum albumin

果糖胺 糖基化 辣木 化学 牛血清白蛋白 果糖 没食子酸 生物化学 单糖 甲基乙二醛 糖苷 糖基化终产物 白蛋白 蛋白质羰基化 食品科学 氧化应激 糖尿病 抗氧化剂 医学 内分泌学 脂质过氧化 有机化学 受体
作者
Pornpimon Nunthanawanich,Weerachat Sompong,Sukrit Sirikwanpong,Kittana Mäkynen,Sirichai Adisakwattana,Winai Dahlan,Sathaporn Ngamukote
出处
期刊:SpringerPlus [Springer Nature]
卷期号:5 (1) 被引量:30
标识
DOI:10.1186/s40064-016-2759-3
摘要

Advanced glycation end products (AGEs) play an important factor for pathophysiology of diabetes and its complications. Moringa oleifera is one of the medicinal plants that have anti-hyperglycemic activity. However, anti-glycation property of Moringa oleifera leaf extract on the different types of reducing monosaccharides-induced protein glycation has not been investigated. Therefore, the aim of this study was to examine the protective effect of Moringa oleifera aqueous leaf extract (MOE) on reducing sugars-induced protein glycation and protein oxidation. Total phenolic content of MOE was measured using the Folin-Ciocalteu method. Bovine serum albumin was incubated with 0.5 M of reducing sugars (glucose or fructose) with or without MOE (0.5-2.0 mg/mL) for 1, 2, 3 and 4 weeks. The results found that total phenolic content was 38.56 ± 1.50 mg gallic acid equivalents/g dry extract. The formation of fluorescent and non-fluorescent AGEs [N (ε)-(carboxymethyl) lysine (CML)] and the level of fructosamine were determined to indicate protein glycation, whereas the level of protein carbonyl content and thiol group were examined for protein oxidation. MOE (0.5-2.0 mg/mL) significantly inhibited the formation of fluorescent, N (ε)-CML and markedly decreased fructosamine level (P < 0.05). Moreover, MOE significantly prevented protein oxidation manifested by reducing protein carbonyl and the depletion of protein thiol in a dose-dependent manner (P < 0.05). Thus, the findings indicated that polyphenols containing in MOE have high potential for decreasing protein glycation and protein oxidation that may delay or prevent AGE-related diabetic complications.
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