کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8301578 | 1537701 | 2016 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Resolvin D1 protects the liver from ischemia/reperfusion injury by enhancing M2 macrophage polarization and efferocytosis
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کلمات کلیدی
ARG1Specialized pro-resolving lipid mediatorsLXSALX/FPR2SPMSResolvinsPMNEfferocytosisIL-1NF-κBLPSCOXPI3KHepatocytes - hepatocytesHPCs - HPC هاResolvin D1 - Resolv D1ROS - ROSRVs - RV هاTLRs - TLR هاarginase 1 - آرژیناز 1cyclooxygenase - آنزیم سیکلواکسیژنازLOX - اکسیژن مایعischemia/reperfusion - ایسکمی / رپرفیوژنinterleukin 1 - اینترلوکین 1tumor necrosis factor alpha - تومور نکروز عامل آلفاResolution of inflammation - حل التهابKupffer cell - سلول کوپفرTNF-α - فاکتور نکروز توموری آلفاnuclear factor kappa B - فاکتور هسته ای کاپا Bphosphoinositide 3-kinase - فسفینوزیتید 3-کینازMacrophage polarization - قطبش ماکروفاژpolymorphonuclear leukocyte - لکوسیت پلی مرفون هسته ایlipoxygenase - لیپواکسیژنازlipopolysaccharide - لیپوپلی ساکاریدLipoxins - لیپوکسین هاReactive oxygen species - گونههای فعال اکسیژنToll-like receptors - گیرنده های پولی مانند
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Resolvin D1 protects the liver from ischemia/reperfusion injury by enhancing M2 macrophage polarization and efferocytosis Resolvin D1 protects the liver from ischemia/reperfusion injury by enhancing M2 macrophage polarization and efferocytosis](/preview/png/8301578.png)
چکیده انگلیسی
Resolution of inflammation is an active process involving a novel category of lipid factors known as specialized pro-resolving lipid mediators, which includes Resolvin D1 (RvD1). While accumulating evidence suggests that RvD1 counteracts proinflammatory signaling and promotes resolution, the specific cellular targets and mechanisms of action of RvD1 remain largely unknown. In the present study, we investigated the role and molecular mechanisms of RvD1 in ischemia/reperfusion (IR)-induced sterile liver inflammation. Male C57BL/6 mice underwent 70% hepatic ischemia for 60 min, followed by reperfusion. RvD1 (5, 10, and 15 μg/kg, i.p.) was administered to the mice 1 h before ischemia and then immediately prior to reperfusion. RvD1 attenuated IR-induced hepatocellular damage and the proinflammatory response. In purified Kupffer cells (KCs) from mice exposed to IR, the levels of M1 marker genes (Nos2a and Cd40) increased, while those of M2 marker genes (Arg1, Cd206, and Mst1r) decreased, demonstrating a proinflammatory shift. RvD1 markedly attenuated these changes. Depletion of KCs by liposome clodronate abrogated the effects of RvD1 on proinflammatory mediators and macrophage polarization. In addition, RvD1 attenuated increases in myeloperoxidase activity and Cxcl1 and Cxcl2 mRNA expression. RvD1 markedly augmented the efferocytic activity of KCs, as indicated by increases in F4/80+ Gr-1+ cells in the liver. However, antagonist pretreatment or gene silencing of the RvD1 receptor, ALX/FPR2, abrogated the anti-inflammatory and pro-resolving actions of RvD1. These data indicate that RvD1 ameliorates IR-induced liver injury, and this protection is associated with enhancement of M2 polarization and efferocytosis via ALX/FPR2 activation.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids - Volume 1861, Issue 9, Part A, September 2016, Pages 1025-1035
Journal: Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids - Volume 1861, Issue 9, Part A, September 2016, Pages 1025-1035
نویسندگان
Jung-Woo Kang, Sun-Mee Lee,