Chia Nan University of Pharmacy & Science Institutional Repository:Item 310902800/27874
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    標題: Interleukin-6 upregulates paraoxonase 1 gene expression via an AKT/NF-kappa B-dependent pathway
    作者: Cheng, Chi-Chih
    Hsueh, Chi-Mei
    Chen, Chiu-Yuan
    Chen, Tzu-Hsiu
    Hsu, Shih-Lan
    貢獻者: 保健營養系
    關鍵字: Paraoxonase 1
    Nf-Kappa B
    日期: 2013-01
    上傳時間: 2014-05-26 10:47:11 (UTC+8)
    出版者: Academic Press Inc Elsevier Science
    摘要: The aim of this study is to investigate the relationship between paraoxonase 1 (PON1) and atherosclerosis-related inflammation. In this study, human hepatoma HepG2 cell line was used as a hepatocyte model to examine the effects of the pro-inflammatory cytokines on PON1 expression. The results showed that IL-6, but not TNF-alpha and IL-1 beta, significantly increased both the function and protein level of PON1; data from real-time RT-PCR analysis revealed that the IL-6-induced PON1 expression occurred at the transcriptional level. Increase of I kappa B kinase activity and I kappa B phosphorylation, and reduction of I kappa B protein level were also observed in IL-6-treated HepG2 cells compared with untreated culture. This event was accompanied by increase of NF-kappa B-p50 and -p65 nuclear translocation. Moreover, treatment with IL-6 augmented the DNA binding activity of NF-kappa B. Furthermore, pharmacological inhibition of NF-kappa B activation by PDTC and BAY 11-7082, markedly suppressed the IL-6-mediated PON1 expression. In addition, IL-6 increased the levels of phosphorylated protein kinase B (PKB, AKT). An AKT inhibitor LY294002 effectively suppressed IKK/I kappa B/NF-kappa B signaling and PON1 gene expression induced by IL-6. Our findings demonstrate that IL-6 upregulates PON1 gene expression through an AKT/NF-kappa B signaling axis in human hepatocyte-derived HepG2 cell line. (c) 2013 Elsevier Inc. All rights reserved.
    關聯: Biochemical And Biophysical Research Communications, v.437 n.1, pp.55-61
    显示于类别:[保健營養系(所) ] 期刊論文
    [食藥產業暨檢測科技系(含五專)] 期刊論文


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