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首页> 外文期刊>International immunopharmacology >p-Coumaric acid inhibits indoleamine 2, 3-dioxygenase expression in murine dendritic cells.
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p-Coumaric acid inhibits indoleamine 2, 3-dioxygenase expression in murine dendritic cells.

机译：对香豆酸抑制小鼠树突状细胞中吲哚胺2、3-二加氧酶的表达。

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摘要

Indoleamine 2, 3-dioxygenase (IDO), a key enzyme that catalyses the initial and rate-limiting step in the degradation of the tryptophan, is simultaneously expressed in murine dendritic cells and macrophages stimulated with interferon-gamma (IFN-gamma). In the present study, we investigated whether p-Coumaric acid (CA), which is suggested to exhibit antioxidant properties, could suppress the functional expression of IDO in murine bone marrow-derived dendritic cells (BMDCs) stimulated with IFN-gamma. Treatment with CA reduced intracellular expression of IDO mRNA and protein levels in IFN-gamma-activated murine BMDCs in vitro and in CD11c(+)CD8alpha(+) DCs of tumor-draining lymph node (TDLN) of tumor-bearing mice in vivo. Consequently, we obtained evidence that CA suppresses the functional activity of IDO, which catalyses oxidative catabolism of tryptophan, and significantly recovers the IDO-dependent T cell suppression. Activation of the signal transducer and activator of transcription 1 (STAT1) is important to be express IDO in IFN-gamma-stimulated murine BMDCs. To determine whether these inhibitory effects of CA are associated with the alteration of the signal transducer and activator of transcription 1 (STAT1) and IFN-gamma-inducible, dsRNA-activated serine/threonine protein kinase (PKR), BMDCs were pretreated with various concentrations of CA. We found that CA inhibited the activation of STAT1 in response to IFN-gamma. Based on our results, this study may account that CA could inhibit IDO expression by down-regulation of STAT1 activation in IFN-gamma-stimulated murine DCs.
机译：吲哚胺2，3-二加氧酶（IDO）是催化色氨酸降解的起始步骤和限速步骤的关键酶，同时在鼠树突状细胞和干扰素-γ（IFN-γ）刺激的巨噬细胞中表达。在本研究中，我们调查了对香豆酸（CA）是否具有抗氧化作用，它是否可以抑制IDO在IFN-γ刺激的小鼠骨髓源性树突状细胞（BMDC）中的功能性表达。用CA处理可以降低体内IFN-γ激活的鼠BMDC和体内引流淋巴结（TDLN）的CD11c（+）CD8alpha（+）DC的IDO mRNA和蛋白水平的细胞内表达。因此，我们获得的证据表明，CA抑制了IDO的功能活性，该活性催化色氨酸的氧化分解代谢，并显着恢复了IDO依赖性T细胞抑制作用。信号转导和转录激活因子1（STAT1）的激活对于在IFN-γ刺激的鼠BMDC中表达IDO至关重要。为了确定CA的这些抑制作用是否与信号转导和转录激活因子1（STAT1）以及IFN-γ诱导的dsRNA激活的丝氨酸/苏氨酸蛋白激酶（PKR）的改变有关，对BMDC进行了不同浓度的预处理的CA。我们发现，CA抑制STAT1对IFN-γ的激活。根据我们的结果，该研究可能说明CA可以通过下调IFN-γ刺激的小鼠DC中STAT1的激活来抑制IDO表达。

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