کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6022064 | 1580662 | 2014 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Nicotinamide pre-treatment ameliorates NAD(H) hyperoxidation and improves neuronal function after severe hypoxia
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کلمات کلیدی
fEPSPPARP-1CA1ROIaCSFSIRT-1HSDNAD(H) - NAD (H)NAD+ - NAD +ROS - ROSstratum radiatum - stratat radiatumcornu ammonis region 1 - آمون منطقه شاخ 1AIF - آیفونReoxygenation - اکسیداسیونdentate gyrus - شکنج دندانه دارapoptosis-inducing factor - عامل القاء آپوپتوزartificial cerebrospinal fluid - مایع مغزی نخاعی مصنوعیBrain - مغزregion of interest - منطقه مورد نظرNAM - نامNAD, nicotinamide adenine dinucleotide - نیکوتینامید آدنین دینوکلئوتیدNicotinamide - نیکوتینامید، نیاسینامیدHippocampus - هیپوکامپ Hypoxia - هیپوکسیfield excitatory post-synaptic potential - پتانسیل پس از سیناپسی مزمن تحریک پذیرPoly(ADP-ribose) polymerase-1 - پلی (ADP-ribose) پلیمراز-1TCA cycle - چرخه TCAtricarboxylic acid cycle - چرخه اسید تریکاربوکیلیکSpreading depression - گسترش افسردگیReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
عصب شناسی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Prolonged hypoxia leads to irreversible loss of neuronal function and metabolic impairment of nicotinamide adenine dinucleotide recycling (between NADÂ + and NADH) immediately after reoxygenation, resulting in NADH hyperoxidation. We test whether the addition of nicotinamide (to enhance NAD+ levels) or PARP-1 inhibition (to prevent consumption of NADÂ +) can be effective in improving either loss of neuronal function or hyperoxidation following severe hypoxic injury in hippocampal slices. After severe, prolonged hypoxia (maintained for 3Â min after spreading depression) there was hyperoxidation of NADH following reoxygenation, an increased soluble NAD+/NADH ratio, loss of neuronal field excitatory post-synaptic potential (fEPSP) and decreased ATP content. Nicotinamide incubation (5Â mM) 2Â h prior to hypoxia significantly increased total NAD(H) content, improved neuronal recovery, enhanced ATP content, and prevented NADH hyperoxidation. The nicotinamide-induced increase in total soluble NAD(H) was more significant in the cytosolic compartment than within mitochondria. Prolonged incubation with PJ-34 (>Â 1Â h) led to enhanced baseline NADH fluorescence prior to hypoxia, as well as improved neuronal recovery, NADH hyperoxidation and ATP content on recovery from severe hypoxia and reoxygenation. In this acute model of severe neuronal dysfunction prolonged incubation with either nicotinamide or PJ-34 prior to hypoxia improved recovery of neuronal function, enhanced NADH reduction and ATP content, but neither treatment restored function when administered during or after prolonged hypoxia and reoxygenation.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neurobiology of Disease - Volume 62, February 2014, Pages 469-478
Journal: Neurobiology of Disease - Volume 62, February 2014, Pages 469-478
نویسندگان
Pavan K. Shetty, Francesca Galeffi, Dennis A. Turner,