کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5703986 | 1602558 | 2017 | 25 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Peptide GC31 inhibits chemokines and ICAM-1 expression in corneal fibroblasts exposed to LPS or poly(I:C) by blocking the NF-κB and MAPK pathways
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کلمات کلیدی
C-type lectin-like domainLPSCTLDDEXFBSFGSMCPICAMinflammation - التهاب( توروم) interferon - اینترفرونIFN - اینترفرون هاinterleukin - اینترلوکینELISA - تست الیزاEnzyme-linked immunosorbent assay - تست الیزاDexamethasone - دگزامتازونfetal bovine serum - سرم جنین گاوlipopolysaccharide - لیپوپلی ساکاریدIntercellular cell adhesion molecule - مولکول چسبندگی سلول بین سلولیmonocyte chemoattractant protein - پروتئین شیمیایی monocyte chemoattractantpoly(I:C) - پلی (I: C)Peptide - پپتید keratocytes - کراتوسیت هاKeratitis - کراتیتChemokines - کرموین ها
موضوعات مرتبط
علوم زیستی و بیوفناوری
ایمنی شناسی و میکروب شناسی
ایمونولوژی و میکروب شناسی (عمومی)
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چکیده انگلیسی
In keratitis, keratocytes play a vital role by releasing inflammatory cytokines and expressing intercellular cell adhesion molecule-1(ICAM-1). GC31 is a peptide derived from thrombomodulin, an endogenous protein with potential anti-inflammation properties. We evaluated the protective effect of GC31 in LPS- or poly(I:C)-induced corneal fibroblasts. Cultured keratocytes were treated with either LPS or poly(I:C); The mRNA and protein expressions of IL-6, IL-8, MCP-1, and IFN-γ were determined by real-time RT-PCR and ELISA. The expression level of ICAM-1 was estimated by real-time RT-PCR, immunofluorescence, and western blot. The underlying pathways were investigated by detecting NF-κB p65 translocation and phosphorylation of IκBα, p65, p38, JNK, and ERK. The MTS assay was used to measure cell viability of keratocytes after GC31 incubation. The elevation of IL-6, IL-8, MCP-1, and IFN-γ expression induced by LPS or poly(I:C) was significantly inhibited by GC31 in a dose-dependent manner at both mRNA and protein levels. GC31 also reduced the expression of ICAM-1 in keratocytes after LPS or poly(I:C) stimulation. LPS or poly(I:C) induced p65 translocation and phosphorylation of IκBα, p65, p38, and JNK were suppressed by GC31.GC31 is not only an effective inhibitor of LPS-induced inflammatory response, but it also inhibits poly(I:C)-induced release of inflammatory cytokines and ICAM-1 expression by blocking the NF-κB and MAPK (p38 and JNK) pathways. This suggested that GC31 may exert a protective effect in attenuating corneal inflammation by suppressing the immune response of the fibroblasts.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Experimental Eye Research - Volume 164, November 2017, Pages 109-117
Journal: Experimental Eye Research - Volume 164, November 2017, Pages 109-117
نویسندگان
Shaopin Zhu, Xun Xu, Kun Liu, Qing Gu, Fang Wei, Huiyi Jin,