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At the interface of antioxidant signalling and cellular function: Key polyphenol effects

机译:在抗氧化剂信号传导和细胞功能的界面:关键的多酚效应

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摘要

The hypothesis that dietary (poly) phenols promote well-being by improving chronic disease-risk biomarkers, such as endothelial dysfunction, chronic inflammation and plasma uric acid, is the subject of intense current research, involving human interventions studies, animal models and in vitro mechanistic work. The original claim that benefits were due to the direct antioxidant properties of (poly) phenols has been mostly superseded by detailed mechanistic studies on specific molecular targets. Nevertheless, many proposed mechanisms in vivo and in vitro are due to modulation of oxidative processes, often involving binding to specific proteins and effects on cell signalling. We review the molecular mechanisms for 3 actions of (poly) phenols on oxidative processes where there is evidence in vivo from human intervention or animal studies. (1) Effects of (poly) phenols on pathways of chronic inflammation leading to prevention of some of the damaging effects associated with the metabolic syndrome. (2) Interaction of (poly) phenols with endothelial cells and smooth muscle cells, leading to effects on blood pressure and endothelial dysfunction, and consequent reduction in cardiovascular disease risk. (3) The inhibition of xanthine oxidoreductase leading to modulation of intracellular superoxide and plasma uric acid, a risk factor for developing type 2 diabetes.
机译:饮食中的(多聚)酚通过改善慢性疾病风险生物标志物(如内皮功能障碍,慢性炎症和血浆尿酸)促进健康的假说是当前研究的主题,涉及人类干预研究,动物模型和体外研究机械工作。最初声称益处是由于(多)酚类化合物的直接抗氧化特性而被主要针对特定​​分子靶标的详细机理研究所取代。尽管如此,体内和体外提出的许多机制是由于氧化过程的调节,通常涉及与特定蛋白质的结合以及对细胞信号传导的影响。我们审查了人类干预或动物研究在体内发现的证据,证明了多酚在氧化过程中的3种作用的分子机制。 (1)(多)酚对慢性炎症途径的作用,导致预防了与代谢综合征相关的某些破坏作用。 (2)(多)酚与内皮细胞和平滑肌细胞的相互作用,导致对血压和内皮功能障碍的影响,并因此降低了心血管疾病的风险。 (3)黄嘌呤氧化还原酶的抑制导致细胞内超氧化物和血浆尿酸的调节,这是发展2型糖尿病的危险因素。

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