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儿茶素抑制糖化牛血清白蛋白消化过程中晚期糖基化终产物的释放及其机制。

Catechin Inhibits the Release of Advanced Glycation End Products during Glycated Bovine Serum Albumin Digestion and Corresponding Mechanisms .

机构信息

Key Laboratory of Fermentation Engineering (Ministry of Education), Hubei Key Laboratoy of Industrial Microbiology, National "111" Center for Cellular Regulation and Molecular Pharmaceutics, Hubei Research Center of Food Fermentation Engineering and Technology, Hubei University of Technology, Wuhan, Hubei 430068, China.

School of Food Science and Engineering, Hainan University/Engineering Research Center of Utilization of Tropical polysaccharide resources, Ministry of Education/Key Laboratory of Food Nutrition and Functional Food of Hainan Province, Haikou 570228, China.

出版信息

J Agric Food Chem. 2021 Aug 11;69(31):8807-8818. doi: 10.1021/acs.jafc.1c03348. Epub 2021 Jul 27.

Abstract

Glycated proteins are the main source of dietary advanced glycation end products (AGEs). Glycated proteins are enzymatically hydrolyzed in the gastrointestinal tract, which releases more absorbable and smaller potentially harmful AGEs. This study investigated the inhibitory effect of catechin on AGE release from glycated bovine serum albumin (G-BSA) during gastrointestinal digestion. Catechin inhibited AGE release during gastrointestinal digestion, especially in the gastric digestion stage. Additionally, catechin altered these peptides in the small intestine by reducing G-BSA digestibility. The proposed mechanism involves interactions between catechin and G-BSA/digestive enzymes, inhibiting digestive enzyme activity and changing the conformation of G-BSA. Catechin reduced G-BSA β-sheet content and protected the helical conformation. Moreover, catechin enhanced the antioxidant capacity of G-BSA, which could attenuate postprandial oxidative stress in the gastrointestinal tract caused by the release of AGEs. This study improves our understanding of the nutritional and health effects of catechin on dietary AGEs during gastrointestinal digestion.

摘要

糖化蛋白是膳食晚期糖基化终产物(AGEs)的主要来源。糖化蛋白在胃肠道中经酶解,释放出更易吸收和更小、潜在更有害的 AGEs。本研究探讨了儿茶素对胃肠道消化过程中糖化牛血清白蛋白(G-BSA)释放 AGE 的抑制作用。儿茶素在胃肠道消化过程中抑制 AGE 释放,特别是在胃消化阶段。此外,儿茶素通过降低 G-BSA 的消化率来改变这些肽在小肠中的存在形式。所提出的机制涉及儿茶素与 G-BSA/消化酶之间的相互作用,抑制消化酶的活性并改变 G-BSA 的构象。儿茶素降低了 G-BSA 的β-折叠含量并保护了螺旋构象。此外,儿茶素增强了 G-BSA 的抗氧化能力,可减轻因 AGE 释放而导致的胃肠道餐后氧化应激。本研究提高了我们对儿茶素在胃肠道消化过程中对膳食 AGE 的营养和健康影响的理解。

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