کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6286495 | 1615394 | 2014 | 20 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Inflammation in intracerebral hemorrhage: From mechanisms to clinical translation
ترجمه فارسی عنوان
التهاب خونریزی داخل مغزی: از مکانیسم تا ترجمه بالینی
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کلمات کلیدی
TIR domain-containing adaptor proteinTLRDAMPsHMGB1MYD88hUCBGFPiNOSNrf2TIRAPRipk3Hypoxia-inducible factor-1aRBCMMP-9MPO - DFOHIF1a - HIF1TRIF - Trif بهEthyl pyruvate - اتیل پیرواتinflammation - التهاب( توروم) TRAM - تراموایTIR - تیرToll-like receptor - تیالآرdanger associated molecular patterns - خطرات مولکولی مرتبط با خطرHuman umbilical cord blood - خون بند ناف انسانintracerebral hemorrhage - خونریزی داخل مغزیBlood–brain barrier - سد خونی مغزیBBB - سد خونی مغزیNeuronal stem cells - سلول های بنیادی عصبیinducible nitric oxide synthase - سنتاز اکسید نیتریک القاییmyeloid differentiation factor 88 - عامل تمایز میلوئید 88NF-E2-related factor-2 - فاکتور 2 مربوط به NF-E2matrix metalloproteinase - ماتریکس متالوپروتئینازICH - منTRIF-related adaptor molecule - مولکول آداپتور مربوط به TRIFmyeloperoxidase - میلوپراکسیداز Microglia - میکروگلیاهاHemoglobin - هموگلوبینheme oxygenase - همگام اکسژنازHigh mobility group box 1 protein - پروتئین جعبه 1 پروتئین گروه تحرکgreen fluorescent protein - پروتئین فلورسنت سبزVascular adhesion protein-1 - پروتئین چسبندگی عروقی-1STICH - کوکred blood cell - گلبول قرمز، اریتروسیت
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
چکیده انگلیسی
Intracerebral hemorrhage (ICH) accounts for 10-15% of all strokes and is associated with high mortality and morbidity. Currently, no effective medical treatment is available to improve functional outcomes in patients with ICH. Potential therapies targeting secondary brain injury are arousing a great deal of interest in translational studies. Increasing evidence has shown that inflammation is the key contributor of ICH-induced secondary brain injury. Inflammation progresses in response to various stimuli produced after ICH. Hematoma components initiate inflammatory signaling via activation of microglia, subsequently releasing proinflammatory cytokines and chemokines to attract peripheral inflammatory infiltration. Hemoglobin (Hb), heme, and iron released after red blood cell lysis aggravate ICH-induced inflammatory injury. Danger associated molecular patterns such as high mobility group box 1 protein, released from damaged or dead cells, trigger inflammation in the late stage of ICH. Preclinical studies have identified inflammatory signaling pathways that are involved in microglial activation, leukocyte infiltration, toll-like receptor (TLR) activation, and danger associated molecular pattern regulation in ICH. Recent advances in understanding the pathogenesis of ICH-induced inflammatory injury have facilitated the identification of several novel therapeutic targets for the treatment of ICH. This review summarizes recent progress concerning the mechanisms underlying ICH-induced inflammation. We focus on the inflammatory signaling pathways involved in microglial activation and TLR signaling, and explore potential therapeutic interventions by targeting the removal of hematoma components and inhibition of TLR signaling.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Progress in Neurobiology - Volume 115, April 2014, Pages 25-44
Journal: Progress in Neurobiology - Volume 115, April 2014, Pages 25-44
نویسندگان
Yu Zhou, Yanchun Wang, Jian Wang, R. Anne Stetler, Qing-Wu Yang,