کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9001636 | 1118539 | 2005 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Neuroprotective effects of TEMPOL in central and peripheral nervous system models of Parkinson's disease
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کلمات کلیدی
4-hydroxy-2,2,6,6-tetramethylpiperidine-N-oxyli.v.DOPACMTSPNAi.p.3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium - 3- (4،5-dimethylthiazol-2-yl) -5- (3-carboxymethoxyphenyl) -2- (4-sulfophenyl) -2H-tetrazoliumAntioxidants - آنتی اکسیدانHomovanilic acid - اسید هومیانیلیکParkinson's disease - بیماری پارکینسونtyrosine hydroxylase - تیروزین هیدروکسیلازintraperitoneal - داخل صفاقیIntravenous - داخل وریدیAutonomic nervous system - دستگاه عصبی خودمختار یا خودگردان یا اتونومDopamine - دوپامینdihydroxyphenylacetic acid - دی هیدروکسی فنیل اسیدهای اسیدTempol - سریعNeuroprotection - محافظت نورونی یا محافظت از عصبHVA - چهReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم پزشکی و سلامت
داروسازی، سم شناسی و علوم دارویی
داروشناسی
پیش نمایش صفحه اول مقاله
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چکیده انگلیسی
TEMPOL (4-hydroxy-2,2,6,6-tetramethylpiperidine-N-oxyl) is a stable nitroxyl antioxidant. Previous studies have suggested that TEMPOL is protective in acute disorders thought to involve reactive oxygen species (ROS), such as ischemic stroke and cardiac reperfusion injury. Oxidized TEMPOL can be recycled to its redox-active reducing form by co-administration with polynitroxylated albumin, making it a candidate as a pharmacological “reservoir” for reducing potential of use in chronic disorders involving ROS. The present studies examine the efficacy of TEMPOL in cell culture and animal models of the central and peripheral dysfunction associated with Parkinson's disease, a disorder in the pathogenesis of which ROS generated from dopamine have been implicated. Antioxidants have been proposed as both preventive and symptomatic therapy for Parkinson's disease. TEMPOL protects MN9D dopaminergic mesencephalic cells in culture from 6-hydroxydopamine (6-OHDA)-induced apoptosis. Translocation of the p65 component of NF-κB to the nucleus accompanies protection by TEMPOL. In vivo, intraperitoneal TEMPOL protects mice from intrastriatal 6-OHDA-induced cell and dopamine metabolite loss in the striatum. TEMPOL also protects mice against the 6-OHDA-induced rotational behavior elicited by intrastriatal administration of d-amphetamine. In addition, TEMPOL protects mice from the ptosis, activity level decrement, and mortality induced by intraperitoneal administration of 6-OHDA, a model of autonomic dysfunction in Parkinson's disease. Adjunctive use of polynitroxylated albumin enhances the in vitro and in vivo effects of TEMPOL.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical Pharmacology - Volume 70, Issue 9, 1 November 2005, Pages 1371-1381
Journal: Biochemical Pharmacology - Volume 70, Issue 9, 1 November 2005, Pages 1371-1381
نویسندگان
Qinghua Liang, Amanda D. Smith, Stephen Pan, Vladimir A. Tyurin, Valerian E. Kagan, Teresa G. Hastings, Nina Felice Schor,