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首页> 外文期刊>RSC Advances >Epigallocatechin gallate prevents senescence by alleviating oxidative stress and inflammation in WI-38 human embryonic fibroblasts
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Epigallocatechin gallate prevents senescence by alleviating oxidative stress and inflammation in WI-38 human embryonic fibroblasts

机译：表没食子儿茶素没食子酸酯通过减轻WI-38人胚成纤维细胞中的氧化应激和炎症来防止衰老

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Increased levels of oxidative stress and inflammation are the underlying mechanisms behind the aging process and age-related diseases. The purpose of our research is to explore whether epigallocatechin gallate (EGCG) can extend replicative life span by preventing the oxidative stress and inflammatory effects of WI-38 fibroblasts and the involved mechanisms in vitro . WI-38 cells were treated with different concentrations of EGCG (0, 25, 50 and 100 μM) at population doubling (PD) 25. At late-stage cells, we determined the age-associated genes with signaling through transcriptome sequencing. The expression profile of the targets in WI-38 fibroblasts was confirmed by bioinformatics analysis, qPCR and western blot. We found that EGCG markedly decreased reactive oxygen species (ROS), and inflammation factors, tumor necrosis factor-α (TNF-α), interleukin (IL)-6, and significantly increased cell proliferation at PD 35 and 45. EGCG treatments significantly decreased p53 and retinoblastoma (Rb) expressions, markedly increased p-Rb and E2F2 expressions as well as antioxidant enzymes and superoxide dismutase (SOD) 1 and SOD2 content, and obviously decreased the expressions of inflammation factors IL-32, TNF-α expressions at PD 45 WI-38 cells. Moreover, the effects were changed by EGCG treatment by p53 siRNA or overexpression. These findings in our studies reveal that EGCG treatments improved senescence and enhanced the replicative life span through alleviating oxidative stress and inflammation in WI-38 fibroblasts.
机译：氧化应激和炎症水平升高是衰老过程和与年龄有关的疾病的潜在机制。我们的研究目的是探讨表没食子儿茶素没食子酸酯（EGCG）是否可以通过防止WI-38成纤维细胞的氧化应激和炎症作用以及相关的体外机制来延长复制寿命。在群体倍增（PD）25处，用不同浓度的EGCG（0、25、50和100μM）处理WI-38细胞。在后期细胞中，我们通过转录组测序确定了与年龄相关的基因。通过生物信息学分析，qPCR和western blot证实了WI-38成纤维细胞中靶标的表达谱。我们发现EGCG显着降低了活性氧（ROS）和炎症因子，肿瘤坏死因子-α（TNF-α），白介素（IL）-6，并显着增加了PD 35和45的细胞增殖。EGCG治疗显着降低了p53和视网膜母细胞瘤（Rb）的表达，p-Rb和E2F2的表达以及抗氧化酶和超氧化物歧化酶（SOD）1和SOD2的含量明显增加，并显着降低PD炎症因子IL-32和TNF-α的表达45个WI-38电池。而且，通过p53 siRNA的EGCG处理或过表达改变了效果。我们研究中的这些发现表明，EGCG治疗可减轻WI-38成纤维细胞的氧化应激和炎症，从而改善衰老并延长复制寿命。

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