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首页> 外文学位 >Regulation of Tumor Necrosis Factor-alpha Signaling in Rheumatoid Arthritis Synovial Fibroblasts by Green Tea Polyphenol Epigallocatechin-3-gallate.
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Regulation of Tumor Necrosis Factor-alpha Signaling in Rheumatoid Arthritis Synovial Fibroblasts by Green Tea Polyphenol Epigallocatechin-3-gallate.

机译：绿茶多酚表没食子儿茶素-3-没食子酸酯对类风湿关节炎滑膜成纤维细胞中肿瘤坏死因子-α信号的调节。

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摘要

Rheumatoid arthritis (RA) is a chronic inflammatory disease, which affects about 1% of the population. It occurs when cytokines, such as interleukin (IL)-1β and tumor necrosis factor (TNF)-&agr;, stimulate synovial fibroblast proliferation leading to joint damage and destruction. Epigallocatechin-3-gallate (EGCG) is a polyphenol found in green tea that has been shown to have an anti-inflammatory effect in RA. Previous studies suggest that EGCG blocks IL-1β signaling pathways to inhibit angiogenesis and tissue destruction in RA. However, little research has been done to determine the effect of EGCG in the TNF-mediated pathways in RA synovial fibroblasts. In these experiments, we investigated the effects EGCG has on the TNF-&agr;-induced signal transduction pathways in RA synovial fibroblasts. In particular, we studied the effect of EGCG on the TNF receptors, TNF Receptor 1 (TNF-R1) and TNF Receptor 2 (TNF-R2), as well as downstream proteins, such as IL-6 and IL-8 in the TNF signaling pathways in RA synovial fibroblasts. We also compared the acute and chronic effects of EGCG on TNF-&agr;-mediated signaling pathways in RA synovial fibroblasts. Results of the study showed that EGCG modestly decreased TNF-R1 and increased TNF-R2 expression. Chronic low dose (100 nM - 1 &mgr;M) pretreatment of RA synovial fibroblasts resulted in a marked dose-dependent inhibition of TNF-&agr;-induced AKT activation. We also observed that EGCG modestly inhibited JNK and p38 with no effect on ERK MAPK in RA synovial fibroblasts. Inhibition of TNF-&agr;-induced downstream signaling pathways by EGCG resulted in decreases in IL-6 and IL-8 production by RA synovial fibroblasts. Overall, the results of this study suggest that EGCG decreases the inflammation and tissue invasion mediated by RA synovial fibroblast inflammatory cytokines via interfering with TNF-&agr; signaling.
机译：类风湿关节炎（RA）是一种慢性炎症性疾病，约占总人口的1％。当白细胞介素（IL）-1β和肿瘤坏死因子（TNF）-α等细胞因子刺激滑膜成纤维细胞增殖导致关节损伤和破坏时，就会发生这种情况。 Epigallocatechin-3-gallate（EGCG）是绿茶中发现的一种多酚，已被证明对RA具有抗炎作用。先前的研究表明，EGCG可以阻断IL-1β信号通路，从而抑制RA中的血管生成和组织破坏。但是，很少有研究确定EGCG在RA滑膜成纤维细胞的TNF介导的途径中的作用。在这些实验中，我们研究了EGCG对RA滑膜成纤维细胞中TNF-α诱导的信号转导途径的影响。特别是，我们研究了EGCG对TNF受体，TNF受体1（TNF-R1）和TNF受体2（TNF-R2）以及下游蛋白（如TNF中的IL-6和IL-8）的影响RA滑膜成纤维细胞中的信号通路。我们还比较了EGCG对RA滑膜成纤维细胞中TNF-α介导的信号通路的急性和慢性作用。研究结果表明，EGCG可适度降低TNF-R1并增加TNF-R2表达。 RA滑膜成纤维细胞的慢性低剂量（100 nM-1和M）预处理导致TNF-α诱导的AKT活化受到明显的剂量依赖性抑制。我们还观察到，EGCG适度抑制JNK和p38，而对RA滑膜成纤维细胞中ERK MAPK没有影响。 EGCG对TNF-α诱导的下游信号通路的抑制导致RA滑膜成纤维细胞IL-6和IL-8产生减少。总体而言，这项研究的结果表明，EGCG可通过干扰TNF-α来减少RA滑膜成纤维细胞炎性细胞因子介导的炎症和组织浸润。信号。

著录项

  • 作者

    Riegsecker, Sharayah.;

  • 作者单位

    The University of Toledo.;

  • 授予单位 The University of Toledo.;
  • 学科 Health Sciences Pharmacology.
  • 学位 M.S.P.S.
  • 年度 2013
  • 页码 74 p.
  • 总页数 74
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

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