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首页> 外文期刊>Journal of Agricultural Science >Green Tea epigallocatechin-3-gallate Protects Against Oxidative Stress-Induced Nuclear Translocation of p53 and Apoptosis in Retinal Pigment Epithelial Cells, ARPE-19
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Green Tea epigallocatechin-3-gallate Protects Against Oxidative Stress-Induced Nuclear Translocation of p53 and Apoptosis in Retinal Pigment Epithelial Cells, ARPE-19

机译:绿茶epigallocatechin-3-gallate可防止氧化应激诱导的p53核易位和视网膜色素上皮细胞凋亡,ARPE-19。

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Epigallocatechin-3-gallate (EGCG), the most abundant polyphenolic flavonoids in green tea has been shown to possess strong antioxidant activities. Oxidative stress causes the defect of retinal pigment epithelial (RPE) cells that contribute to several retinal diseases. Several studies have shown that increasing the body’s defenses against oxidative stress with specific antioxidants and mineral supplements could preserve the vision. Therefore, the purpose of this study was to determine the protective role of EGCG against exogenous reactive oxygen species hydrogen peroxide (H2O2)-induced cell death in ARPE-19 cells, human retinal pigment epithelial cell line. ARPE-19 cells were pretreated with EGCG in the presence/absence of H2O2. The protective effects of EGCG and the underlined mechanisms against H2O2 were evaluated. The present study demonstrated that 400 μM H2O2 significantly decreased cell viability, increased the accumulation of intracellular reactive oxygen species (ROS) and increased the number of terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL)-positive cells and chromatin condensed nuclei. In addition, H2O2 induced p53 nuclear translocation, up-regulated Bax and down-regulated Bcl-2 expression thereby increased Bax/Bcl-2 ratio. These toxic effects of H2O2 were reversed by 100 μM EGCG pretreatment. These studies suggest that EGCG protects H2O2-induced cell death in ARPE-19 cells by its antioxidant property and attenuation of p53 nuclear translocation.
机译:Epigallocatechin-3-gallate(EGCG)是绿茶中最丰富的多酚类黄酮,已被证明具有很强的抗氧化活性。氧化应激导致视网膜色素上皮细胞(RPE)的缺陷,导致多种视网膜疾病。多项研究表明,通过使用特定的抗氧化剂和矿物质补充剂来增强人体抵抗氧化应激的防御能力,可以保留视力。因此,本研究的目的是确定EGCG对ARPE-19细胞,人视网膜色素上皮细胞系中外源性活性氧过氧化氢(H2O2)诱导的细胞死亡的保护作用。在有/无H2O2的情况下,用EGCG预处理ARPE-19细胞。评估了EGCG的保护作用和对H2O2的强调机制。本研究表明400μMH2O2显着降低了细胞活力,增加了细胞内活性氧(ROS)的积累并增加了末端脱氧核苷酸转移酶dUTP缺口末端标记(TUNEL)阳性细胞和染色质浓缩核的数量。此外,H2O2诱导了p53核易位,Bax上调和Bcl-2表达下调,从而增加了Bax / Bcl-2比率。通过100μMEGCG预处理可以逆转H2O2的这些毒性作用。这些研究表明,EGCG通过其抗氧化特性和p53核易位的减弱来保护ARPE-19细胞中H2O2诱导的细胞死亡。

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