کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10144137 | 1646296 | 2018 | 37 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Apoptosis Signal-regulating Kinase 1 Silencing on Astroglial Inflammasomes in an Experimental Model of Ischemic Stroke
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کلمات کلیدی
PBSTNFNucleotide-binding oligomerization domain-like receptorNLRASK1OGDDAPIGFAPNOD4′,6-diamidino-2-phenylindole - 4 '، 6-دیامیدینو-2-فنیلینولBSA - BSADMSO - DMSOOGD/R - OGD / RAstrocyte - آستروسیتbovine serum albumin - آلبومین سرم گاوamyotrophic lateral sclerosis - اسکلروز جانبی آمیوتروفیکinflammasomes - التهابinterleukin - اینترلوکینALS - بیماری اسکلروز جانبی آمیوتروفیکTerminal deoxynucleotidyl transferase dUTP nick end labeling - ترمینال deoxynucleotidyl transferase dUTP نام نهایی پایان نامهTUNEL - تونلnucleotide-binding oligomerization domain - دامنه oligomerization اتصال دهنده نوکلئوتیدCNS - دستگاه عصبی مرکزیDimethyl sulfoxide - دیمتیل سولفواکسیدIschemic stroke - سکته مغزی ایسکمیکcentral nervous system - سیستم عصبی مرکزیtumor necrosis factor - فاکتور نکروز تومورOxygen glucose deprivation - محرومیت گلوکز اکسیژنPhosphate-buffered saline - محلول نمک فسفات با خاصیت بافریInflammatory response - واکنش التهابیGlial fibrillary acidic protein - پروتئین اسیدی فیبریلاسیون گلایالapoptosis signal-regulating kinase 1 - کیناز تنظیم کننده سیگنال آپوپتوز 1
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Activation of the inflammasome complex contributes to the inflammatory response and cell death under pathologic conditions. The nucleotide-binding oligomerization domain-like receptor pyrin domain-containing 2 (NLRP2) inflammasome is activated in astrocytes after cerebral ischemia, which can aggravate ischemic damage. Apoptosis signal-regulating kinase 1 (ASK1) is an early activator and immune-regulator after ischemic injury, that can lead to cell death. The objective of the present study was to evaluate the role of ASK1 in controlling NLRP2 inflammasomes in astrocytes after cerebral ischemia. In a mouse model of ischemic stroke, the levels of NLRP2 inflammasome components, and interleukin (IL)-1β and IL-18, were quantified in different brain regions. In addition, an astrocyte cell line was subjected to oxygen-glucose deprivation and reperfusion (OGD/R) injury, and the levels of NLRP2 inflammasome factors, IL-1β and IL-18 were evaluated. Ischemic brain injury activated astrocytes. The levels of NLRP2 inflammasome components, IL-1β and IL-18 productions, and cell death increased in the cortex and striatum after ischemic injury. In cultured astrocytes, NLRP2 inflammasome components, IL-1β and IL-18 levels were upregulated after OGD/R. ASK1 silencing or inhibition efficiently reduced NLRP2 inflammasome components and pro-inflammatory cytokine levels in mice and cultured astrocytes. Our findings identify a key role for ASK1 in regulating astroglial inflammasomes after cerebral ischemia. We suggest ASK1 as one of the main targets for astroglial inflammasomes in ischemic stroke.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 390, 15 October 2018, Pages 218-230
Journal: Neuroscience - Volume 390, 15 October 2018, Pages 218-230
نویسندگان
So Yeong Cheon, Eun Jung Kim, So Yeon Kim, Jeong Min Kim, Eun Hee Kam, Jong-Kwang Park, Bon-Nyeo Koo,