کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8840755 | 1614697 | 2018 | 32 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Inhibitive Effect of Resveratrol on the Inflammation in Cultured Astrocytes and Microglia Induced by Aβ1-42
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کلمات کلیدی
NF-κBinhibitor kappa BPDTCIP-10MHC IIβ-site APP cleaving enzyme 1CD40CCKIκBIL-1βAPCDAPIMCP-1iNOSIBALPSAβBACE1GFAP4′,6-diamidino-2-phenylindole - 4 '، 6-دیامیدینو-2-فنیلینولMAPK - MAPKantigen-presenting cell - آنتیژن ارائه سلولInterleukin-1β - اینترلوکین-1βBeta-amyloid - بتا آمیلوئیدAlzheimer’s disease - بیماری آلزایمرcluster of differentiation 40 - خوشه تمایز 40CNS - دستگاه عصبی مرکزیpyrrolidine dithiocarbamate - دی اتیل کربامات پیرولیدینBlood–brain barrier - سد خونی مغزیBBB - سد خونی مغزیinducible nitric oxide synthase - سنتاز اکسید نیتریک القاییcentral nervous system - سیستم عصبی مرکزیendoplasmic reticulum - شبکه آندوپلاسمی nuclear factor kappa B - فاکتور هسته ای کاپا Blipopolysaccharide - لیپوپلی ساکاریدNitric oxide - نیتریک اکسیدmonocyte chemotactic protein 1 - پروتئین chemotactic monocyte 1Glial fibrillary acidic protein - پروتئین اسیدی فیبریلاسیون گلایالInterferon-inducible protein-10 - پروتئین القا کننده اینترفرون 10mitogen-activated protein kinase - پروتئین کیناز فعال با mitogenoptical density - چگالی نوریMajor histocompatibility complex class II - کلاس پیچیده بافتی عمده II
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Astrocytes and microglia appear central to the initiation and progression of neuroinflammation in Alzheimer's disease (AD). In this study, inflammation was mimicked by Aβ1-42 treatment of rat astrocytes (RA) and N9 microglia cell lines. Inflammation induced by Aβ1-42 can be inhibited by pyrrolidine dithiocarbamic acid (PDTC), indicating that the NF-κB signal pathway is involved in inflammation. Then, the inhibitive effects of resveratrol (Res) on the inflammation in RA and N9 cells were assessed by observing the changes in inflammatory factors, chemokines, cell cycle and adhesion molecules on the cell surface. 17β-Estradiol was used as an estrogen-positive control because Res is one of the selective estrogen receptor modulators. In RA cells, TNF-α, IL-1β and MCP-1 in the supernatant and the proliferation index in the cell cycle were decreased by 5, 12.5, and 25â¯Î¼M Res and 20â¯nM 17β-estradiol treatment 24â¯h before Aβ1-42. Similarly, in N9 microglial, the levels of IL-1β, IL-6 and NO in the supernatant and CD40 and MHCII in the 10, 20, and 40â¯Î¼M Res and 20â¯nM 17β-estradiol treatment groups decreased markedly compared with the Aβ1-42 treatment group. In addition, Res decreased the nuclear translocation of NF-κB/p65 when checked by immunofluorescence. Furthermore, Res increased the expression of NF-κB/p65 and decreased the expression of p-IκB in the cytoplasm in both RA and N9 microglia. Taken together, the present data indicate that Res reduces inflammation in RA and N9 microglia, and the anti-NF-κB signal pathway may be one of the target mechanisms.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 379, 21 May 2018, Pages 390-404
Journal: Neuroscience - Volume 379, 21 May 2018, Pages 390-404
نویسندگان
Haifeng Zhao, Qian Wang, Xuejiao Cheng, Xuemin Li, Na Li, Tiantian Liu, Jing Li, Qian Yang, Ruirui Dong, Yusen Zhang, Luping Zhang,