Suppr超能文献

棘白菌素抑制人白细胞介素 1β刺激的成纤维样滑膜细胞产生粒细胞集落刺激因子。

Aciculatin inhibits granulocyte colony-stimulating factor production by human interleukin 1β-stimulated fibroblast-like synoviocytes.

机构信息

Orthopedic Department, Shin Kong Wu Ho-Su Memorial Hospital, Taipei, Taiwan.

出版信息

PLoS One. 2012;7(7):e42389. doi: 10.1371/journal.pone.0042389. Epub 2012 Jul 31.

Abstract

The expression of granulocyte colony-stimulating factor (G-CSF), the major regulator of neutrophil maturation, by human fibroblast-like synoviocytes (FLS) can be stimulated by the inflammatory cytokine interleukin-1β (IL-1β). G-CSF is known to contribute to the pathologic processes of destructive arthritis, but the induction mechanism remains unknown. The aims of this study were to identify the signaling pathways involved in IL-1β-stimulated G-CSF production and to determine whether this process was inhibited by aciculatin (8-((2R,4S,5S,6R)-tetrahydro-4,5-dihydroxy-6-methyl-2H-pyran-2-yl)-5-hydroxy-2-(4-hydroxyphenyl)-7-methoxy-4H-chromen-4-one), the major bioactive component of Chrysopogon aciculatus. IL-1β-induced cytokine expression was evaluated by measuring mRNA and protein levels by RT-PCR, ELISA, and Milliplex® assay. Whether aciculatin inhibited IL-1β-stimulated G-CSF expression, and if so, how, were evaluated using western blot assay, an electrophoretic mobility shift assay, and a reporter gene assay. Neutrophil differentiation was determined by Wright-Giemsa staining and flow cytometry. Aciculatin markedly inhibited G-CSF expression induced by IL-1β (10 ng/mL) in a concentration-dependent manner (1-10 µM). In clarifying the mechanisms involved, aciculatin was found to inhibit the IL-1β-induced activation of the IκB kinase (IKK)/IκB/nuclear factor-κB (NF-κB) and mitogen-activated protein kinase (MAPK) pathways by suppressing the DNA binding activity of the transcription factors NF-κB and activator protein (AP)-1. Furthermore, aciculatin significantly inhibited the G-CSF-mediated phosphorylation of Janus kinase-signal transducer and activator of transcription (JAK-STAT) and Akt and neutrophil differentiation from precursor cells. Our results show that aciculatin inhibits IL-1β-stimulated G-CSF expression and the subsequent neutrophil differentiation, suggesting that it might have therapeutic potential for inflammatory arthritis.

摘要

人成纤维样滑膜细胞(FLS)中粒细胞集落刺激因子(G-CSF)的表达可被炎症细胞因子白细胞介素-1β(IL-1β)刺激。已知 G-CSF 有助于破坏性关节炎的病理过程,但诱导机制尚不清楚。本研究旨在鉴定参与 IL-1β刺激 G-CSF 产生的信号通路,并确定该过程是否被 Chrysopogon aciculatus 的主要生物活性成分 aciculatin(8-((2R,4S,5S,6R)-四氢-4,5-二羟基-6-甲基-2H-吡喃-2-基)-5-羟基-2-(4-羟基苯基)-7-甲氧基-4H-色烯-4-酮)抑制。通过 RT-PCR、ELISA 和 Milliplex®测定评估细胞因子表达的 mRNA 和蛋白水平。通过 Western blot 测定、电泳迁移率变动测定和报告基因测定评估 aciculatin 是否抑制 IL-1β 刺激的 G-CSF 表达,如果是,如何抑制。通过 Wright-Giemsa 染色和流式细胞术测定中性粒细胞分化。Aciculatin 以浓度依赖性方式(1-10 μM)显着抑制由 IL-1β(10ng/mL)诱导的 G-CSF 表达。在阐明所涉及的机制时,发现 aciculatin 通过抑制转录因子 NF-κB 和激活蛋白(AP)-1 的 DNA 结合活性来抑制 IL-1β 诱导的 IκB 激酶(IKK)/IκB/核因子-κB(NF-κB)和丝裂原活化蛋白激酶(MAPK)途径的激活。此外,aciculatin 显着抑制 G-CSF 介导的 Janus 激酶信号转导和转录激活因子(JAK-STAT)和 Akt 的磷酸化以及前体细胞向中性粒细胞的分化。我们的结果表明,aciculatin 抑制 IL-1β 刺激的 G-CSF 表达和随后的中性粒细胞分化,表明其可能对炎症性关节炎具有治疗潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0351/3409160/0815c987b779/pone.0042389.g001.jpg

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验