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茶多酚(黄烷-3-醇衍生物)对铜离子介导的低密度脂蛋白氧化修饰的抑制作用。

The inhibitory effects of tea polyphenols (flavan-3-ol derivatives) on Cu2+ mediated oxidative modification of low density lipoprotein.

作者信息

Miura S, Watanabe J, Tomita T, Sano M, Tomita I

机构信息

School of Pharmaceutical Sciences, University of Shizuoka, Japan.

出版信息

Biol Pharm Bull. 1994 Dec;17(12):1567-72. doi: 10.1248/bpb.17.1567.

DOI:10.1248/bpb.17.1567
PMID:7735196
Abstract

Tea polyphenols (flavan-3-ol derivatives) suppressed the oxidative modification of low density lipoprotein (LDL) which is assumed to be an important step in the pathogenesis of atherosclerosis lesions. Inhibitory experiments on the oxidative impairment of porcine serum LDL by flavan-3-ols were carried out by incubating them at 37 degrees C in the presence of 5 microM Cu2+. The oxidation of LDL was monitored either by an absorption increase at 234 nm due to the conjugated diene formation, or the formation of hydroperoxides and thiobarbituric acid reactive substances (TBARS). It was found that the oxidation was strongly inhibited by various flavan-3-ols, and a lag time over 100 min appeared, depending on the types of flavan-3-ols used. The activities based on the prolongation of the lag time were in the order of (-)-epigallocatechin (EGC) < (+)-catechin (C) < (-)-epicatechin (EC) < (-)-epicatechingallate (ECG) < (-)-epigallocatechingallate (EGCG). IC50 of flavan-3-ols on Cu2+ mediated hydroperoxides and TBARS formation of LDL were 0.90, 0.95 microM for ECG and 2.38, 2.74 microM for EGC, respectively. It was found that the Cu2+ mediated cholesterol ester degradation in LDL was almost completely inhibited by 5.0 microM C or EGCG. Cu2+ mediated apolipoprotein B-100 fragmentation was also inhibited (up to 60%) in the presence of C or EGCG.

摘要

茶多酚(黄烷 - 3 - 醇衍生物)可抑制低密度脂蛋白(LDL)的氧化修饰,而这种氧化修饰被认为是动脉粥样硬化病变发病机制中的一个重要步骤。通过在5 microM Cu2+存在下于37摄氏度孵育黄烷 - 3 - 醇,对猪血清LDL的氧化损伤进行了抑制实验。通过监测234 nm处由于共轭二烯形成导致的吸光度增加,或氢过氧化物和硫代巴比妥酸反应性物质(TBARS)的形成来监测LDL的氧化。结果发现,各种黄烷 - 3 - 醇均能强烈抑制氧化反应,并且根据所使用的黄烷 - 3 - 醇类型,出现了超过100分钟的延迟时间。基于延迟时间延长的活性顺序为( - ) - 表没食子儿茶素(EGC)<( + ) - 儿茶素(C)<( - ) - 表儿茶素(EC)<( - ) - 表儿茶素没食子酸酯(ECG)<( - ) - 表没食子儿茶素没食子酸酯(EGCG)。黄烷 - 3 - 醇对Cu2+介导的LDL氢过氧化物和TBARS形成的IC50分别为ECG的0.90、0.95 microM和EGC的2.38、2.74 microM。结果发现,5.0 microM的C或EGCG几乎完全抑制了Cu2+介导的LDL中胆固醇酯的降解。在C或EGCG存在下,Cu2+介导的载脂蛋白B - 100片段化也受到抑制(高达60%)。

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