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绿茶多酚表没食子儿茶素没食子酸酯通过诱导 SOCS1 基因表达抑制细胞信号转导。

Green tea polyphenol epigallocatechin gallate inhibits cell signaling by inducing SOCS1 gene expression.

机构信息

Laboratory of Immune Regulation, Graduate School of Frontier Biosciences, Osaka University, Osaka 565-0871, Japan.

出版信息

Int Immunol. 2010 May;22(5):359-66. doi: 10.1093/intimm/dxq015. Epub 2010 Feb 26.

Abstract

Therapeutic effects of green tea involve an inhibitory function of its constituent polyphenol epigallocatechin gallate (EGCG) on cell signaling. The specificity and mechanism(s) by which EGCG inhibits cell signaling have remained unclear. Here, we demonstrate that green tea and EGCG induce suppressor of cytokine signaling 1 (SOCS1) gene expression, a negative regulator of specific cell signaling pathways. In mouse immune cells, EGCG induces SOCS1 expression via an oxidative (superoxide) pathway and activation of the signal transducer and activator of transcription 5 transcription factor. EGCG inhibited SOCS1-regulated cell signaling, but this inhibitory effect was abrogated in cells deficient in SOCS1. These findings identify a mechanism by which EGCG inhibits cell signaling with specificity, mediated by induction of the negative regulator SOCS1.

摘要

绿茶的治疗作用涉及其组成多酚表没食子儿茶素没食子酸酯(EGCG)对细胞信号的抑制功能。EGCG 抑制细胞信号的特异性和机制尚不清楚。在这里,我们证明绿茶和 EGCG 诱导细胞因子信号转导抑制因子 1(SOCS1)基因表达,这是特定细胞信号通路的负调节剂。在小鼠免疫细胞中,EGCG 通过氧化(超氧)途径和信号转导和转录激活因子 5 转录因子的激活诱导 SOCS1 表达。EGCG 抑制 SOCS1 调节的细胞信号,但在 SOCS1 缺陷细胞中这种抑制作用被消除。这些发现确定了 EGCG 抑制细胞信号的机制,具有特异性,由负调节剂 SOCS1 的诱导介导。

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