首页> 外文期刊>Molecular medicine reports >Impact of epigallocatechin-3-gallate on expression of nuclear factor erythroid 2-related factor 2 and gamma-glutamyl cysteine synthetase genes in oxidative stress-induced mouse renal tubular epithelial cells
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Impact of epigallocatechin-3-gallate on expression of nuclear factor erythroid 2-related factor 2 and gamma-glutamyl cysteine synthetase genes in oxidative stress-induced mouse renal tubular epithelial cells

机译:EpigallocateChin-3-gallate对氧化应激诱导小鼠肾小管上皮细胞核因子红细胞2相关因子2和γ-谷氨酸半胱氨酸合成酶基因的影响

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摘要

The aim of the present study was to investigate the antioxidant response mechanism of epigallocatechin-3-gallate (EGCG) in H2O2-induced mouse renal tubular epithelial cells (MRTECs). The cultured MRTECs were divided into normal, H2O2 (control) and EGCG treatment groups. The MTT assay was used to assess cell viability, and reverse transcription-quantitative polymerase chain reaction (RT-qPCR), immunocytochemical and western blot analyses were performed to detect the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and -glutamyl cysteine synthetase (-GCS). EGCG was able to mitigate H2O2-mediated cell damage. The RT-qPCR results demonstrated that EGCG was able to upregulate the gene expression of Nrf2 and -GCS in MRTECs in a dose-dependent manner. The immunocytochemistry and western blot analyses demonstrated that EGCG was able to increase the protein expression of Nrf2 and -GCS in MRTECs in a dose-dependent manner. Oxidative stress may lead to a decrease in the viability of MRTECs, while EGCG was able to promote the expression of Nrf2 and -GCS in MRTECs, thereby improving the antioxidant capacity of the cells and promoting the repair of oxidative stress injury.
机译:本研究的目的是调查在H 2 O 2诱导的小鼠肾小管上皮细胞(MRTECs)没食子儿茶素-3-没食子酸酯(EGCG)的抗氧化反应机制。将培养MRTECs分为正常,H2O2(对照)和EGCG处理组。 MTT测定来评估细胞生存力,以及反转录定量聚合酶链式反应(RT-qPCR的),进行免疫细胞化学和免疫印迹分析来检测核因子的红系2相关因子2(Nrf2的)和表达式谷氨酰半胱氨酸合成(-GCS)。 EGCG能减轻H2O2介导的细胞损伤。所述RT-qPCR的结果表明,EGCG能够上调的Nrf2和-GCS的基因表达在MRTECs以剂量依赖的方式。免疫细胞化学和免疫印迹分析表明,EGCG能够增加Nrf2的和-GCS的蛋白表达在MRTECs以剂量依赖的方式。氧化应激可导致MRTECs的存活力降低,而EGCG能够促进的Nrf2和-GCS的表达MRTECs,从而提高了细胞的抗氧化能力和促进氧化应激损伤的修复。

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