کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10758456 | 1050407 | 2013 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Procyanidin dimer B2-mediated IRAK-M induction negatively regulates TLR4 signaling in macrophages
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کلمات کلیدی
PBSLPSIκ-BSDSFITCSOCS1MYD88DTTPMSFNF-κBMAPK - MAPKinterferon - اینترفرونIFN - اینترفرون هاinterleukin - اینترلوکینTIR - تیرdithiothreitol - دیتیوتریتولsodium dodecyl sulfate - سدیم دودسیل سولفاتsuppressor of cytokine signaling 1 - سرکوب کننده سیگنالینگ سیتوکین 1myeloid differentiation factor 88 - عامل تمایز میلوئید 88IRAK - عراقnuclear factor-κB - فاکتور هسته ای κBphycoerythrin - فایکوئیریدینfluorescein isothiocyanate - فلوئورسین ایسوتیوسیاناتPhenylmethanesulfonyl fluoride - فنیل متیل سولفونیل فلورایدlipopolysaccharide - لیپوپلی ساکاریدPhosphate-buffered saline - محلول نمک فسفات با خاصیت بافریinhibitor of κB - مهار کننده κBmitogen-activated protein kinase - پروتئین کیناز فعال با mitogenIL-1 receptor-associated kinase - کیناز مرتبط با گیرنده IL-1
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Polyphenolic compounds have been found to possess a wide range of physiological activities that may contribute to their beneficial effects against inflammation-related diseases; however, the molecular mechanisms underlying this anti-inflammatory activity are not completely characterized, and many features remain to be elucidated. In this study, we investigated the molecular basis for the down-regulation of toll-like receptor 4 (TLR4) signal transduction by procyanidin dimer B2 (Pro B2) in macrophages. Pro B2 markedly elevated the expression of the interleukin (IL)-1 receptor-associated kinase (IRAK)-M protein, a negative regulator of TLR signaling. Lipopolysaccharide (LPS)-induced expression of cell surface molecules (CD80, CD86, and MHC class I/II) and production of pro-inflammatory cytokines (tumor necrosis factor-α, IL-1β, IL-6, and IL-12p70) were inhibited by Pro B2, and this action was prevented by IRAK-M silencing. In addition, Pro B2-treated macrophages inhibited LPS-induced activation of mitogen-activated protein kinases such as extracellular signal-regulated kinase 1/2, p38, and c-Jun N-terminal kinase and the translocation of nuclear factor κB and p65 through IRAK-M. We also found that Pro B2-treated macrophages inactivated naïve T cells by inhibiting LPS-induced interferon-γ and IL-2 secretion through IRAK-M. These novel findings provide new insights into the understanding of negative regulatory mechanisms of the TLR4 signaling pathway and the immune-pharmacological role of Pro B2 in the immune response against the development and progression of many chronic diseases.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 438, Issue 1, 16 August 2013, Pages 122-128
Journal: Biochemical and Biophysical Research Communications - Volume 438, Issue 1, 16 August 2013, Pages 122-128
نویسندگان
Nak-Yun Sung, Mi-So Yang, Du-Sub Song, Jae-Kyung Kim, Jong-Heum Park, Beom-Seok Song, Sang-Hyun Park, Ju-Woon Lee, Hyun-Jin Park, Jae-Hun Kim, Eui-Baek Byun, Eui-Hong Byun,