کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6271804 | 1614773 | 2015 | 12 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Harpagoside ameliorates the amyloid-β-induced cognitive impairment in rats via up-regulating BDNF expression and MAPK/PI3K pathways
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کلمات کلیدی
NMDADABDMEMTBSTGDNFAβTrkBERKBCAPI3-kinaseN-methyl-d-aspartate3,3′-diaminobenzidine - 3،3'-diaminobenzidineBDNF - BDNF یا فاکتور نورونزایی مشتقشده از مغز Dulbecco’s modified Eagle medium - Modified Eagle اصلاح شده Dulbeccop-Akt - P-AKTp-ERK1/2 - P-ERK1 / 2Tris-buffered saline with Tween 20 - Tris-buffered saline با Tween 20β-Amyloid - β-آمیلوئیدAChE - آهیAcetylcholinesterase - استیل کولین استرازHAR - اندbicinchoninic acid - بیسینکنینیک اسیدAlzheimer’s disease - بیماری آلزایمرEnzyme-linked immunosorbent assay - تست الیزاELISA - تست الیزاBrain-derived neurotrophic factor (BDNF) - فاکتور نوروئرتفیک مغزی (BDNF)Glial cell line-derived neurotrophic factor - فاکتور نوروتروفی مشتق از سلول گلیاییBrain-derived neurotrophic factor - فاکتور نوروتروفی مشتق شده از مغزPhosphatidylinositol 3-kinase - فسفاتیدیلینواستیل 3-کینازHarpagoside - هارپاگوزیدHydroxypropyl methyl cellulose - هیدروکسی پروپیل متیل سلولزextracellular-regulated protein kinase - پروتئین کیناز کنترل شده خارج سلولیChAT - چتcholine acetyltransferase - کولین استیل ترانسفرازtyrosine receptor kinase B - گیرنده تریروزین کیناز بLearning and memory deficits - یادگیری و کمبود حافظه
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
So far, no effective disease-modifying therapies for Alzheimer's disease (AD) aiming at protecting or reversing neurodegeneration of the disease have been established yet. The present work aims to elucidate the effect of Harpagoside (abbreviated HAR), an iridoid glycosides purified from the Chinese medicinal herb Scrophularia ningpoensis, on neurodegeneration induced by β-amyloid peptide (Aβ) and the underlying molecular mechanism. Here we show that HAR exerts neuroprotective effects against Aβ neurotoxicity. Rats injected aggregated Aβ1-40 into the bilateral hippocampus displayed impaired spatial learning and memory ability in a Y-maze test and novel object recognition test, while HAR treatment ameliorated Aβ1-40-induced behavioral deficits. Moreover, administration of HAR increased the expression levels of brain-derived neurotrophic factor (BDNF) and activated the extracellular-regulated protein kinase (ERK) and the phosphatidylinositol 3-kinase (PI3-kinase) pathways both in the cerebral cortex and hippocampus of the Aβ1-40-insulted rat model. Furthermore, in cultured primary cortical neurons, Aβ1-42 induced significant decrease of choline acetyltransferase (ChAT)-positive neuron number and neurite outgrowth length, both of which were dose dependently increased by HAR. In addition, HAR pretreatment also significantly attenuated the decrease of cell viability in Aβ1-42-injured primary cortical neurons. Finally, when K252a, an inhibitor of Trk tyrosine kinases, and a BDNF neutralizing antibody were added to the culture medium 2 h prior to HAR addition, the protective effect of HAR on Aβ1-42-induced neurodegeneration in the primary cortical neuron was almost inhibited. Taken together, HAR exerting neuroprotection effect and ameliorating learning and memory deficit appears to be associated, at least in part, with up-regulation of BDNF content as well as activating its downstream signaling pathways, e.g., MAPK/PI3K pathways. It raises the possibility that HAR has potential to be a therapeutic agent against AD.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 303, 10 September 2015, Pages 103-114
Journal: Neuroscience - Volume 303, 10 September 2015, Pages 103-114
نویسندگان
J. Li, X. Ding, R. Zhang, W. Jiang, X. Sun, Z. Xia, X. Wang, E. Wu, Y. Zhang, Y. Hu,