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茶儿茶素对2型糖尿病红细胞氧化损伤的保护作用。

Protective role of tea catechins against oxidation-induced damage of type 2 diabetic erythrocytes.

作者信息

Rizvi Syed Ibrahim, Zaid Mohd Abu, Anis Rafat, Mishra Neetu

机构信息

Department of Biochemistry, University of Allahabad, Allahabad, India.

出版信息

Clin Exp Pharmacol Physiol. 2005 Jan-Feb;32(1-2):70-5. doi: 10.1111/j.1440-1681.2005.04160.x.

Abstract
  1. Oxidative stress is recognized as a major contributing factor for the development of late complications of diabetes. 2. Tea contains polyphenolic compounds (catechins), which have many important biological properties, including strong anti-oxidant activity. 3. The present study was undertaken to evaluate the effect of tea catechins (epigallocatechin gallate (EGCG), epigallocatechin (EGC), epicatechin gallate (ECG) and epicatechin (EC)) on markers of oxidative stress (malondialdehyde (MDA), reduced glutathione (GSH) and membrane -SH group) in erythrocytes from type 2 diabetics. 4. Oxidative stress was induced in normal and type 2 diabetic erythrocytes by incubating with tert-butyl hydroperoxide (t-BHP). 5. Diabetic erythrocytes have higher MDA and decreased GSH and membrane -SH groups compared with normal erythrocytes. 6. Our results show that tea catechins protect erythrocytes from t-BHP-induced oxidative stress, the effect being more pronounced in diabetic erythrocytes. The relative effectiveness of individual catechins are in the order of EGCG>ECG>EGC>EC. 7. We hypothesise that a higher intake of catechin-rich food by diabetic patients may provide some protection against the development of long-term complications of diabetes.
摘要
  1. 氧化应激被认为是糖尿病晚期并发症发生的一个主要促成因素。2. 茶含有多酚类化合物(儿茶素),这些化合物具有许多重要的生物学特性,包括强大的抗氧化活性。3. 本研究旨在评估茶儿茶素(表没食子儿茶素没食子酸酯(EGCG)、表没食子儿茶素(EGC)、表儿茶素没食子酸酯(ECG)和表儿茶素(EC))对2型糖尿病患者红细胞氧化应激标志物(丙二醛(MDA)、还原型谷胱甘肽(GSH)和膜-SH基团)的影响。4. 通过与叔丁基过氧化氢(t-BHP)孵育,在正常和2型糖尿病红细胞中诱导氧化应激。5. 与正常红细胞相比,糖尿病红细胞的MDA含量更高,GSH和膜-SH基团减少。6. 我们的结果表明,茶儿茶素可保护红细胞免受t-BHP诱导的氧化应激,这种作用在糖尿病红细胞中更为明显。各儿茶素的相对有效性顺序为EGCG>ECG>EGC>EC。7. 我们假设糖尿病患者摄入更多富含儿茶素的食物可能为预防糖尿病长期并发症的发生提供一些保护。

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