کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
3840094 | 1247889 | 2015 | 21 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Amelioration of nicotinamide adenine dinucleotide phosphate-oxidase mediated stress reduces cell death after blast-induced traumatic brain injury
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کلمات کلیدی
EPMdiaminobenzadineTBIWWEPHFNFLNIHSTDHO-1NADPHDNPHCTRLmRNACTEDAB2,4-dinitrophenylhydrazine - 2،4-dinitrophenylhydrazineNOx - NOXROS - ROSTraumatic brain injury - آسیب تروماتیک مغزStandard - استانداردchronic traumatic encephalopathy - انسفالوپاتی مزمن ترومایتیNADPH oxidase - اکسیداز NADPH Immunohistochemistry - ایمونوهیستوشیمیIHC - ایمونوهیستوشیمیelevated plus maze - بالا به همراه پیچ و خمanalysis of variance - تحلیل واریانسANOVA - تحلیل واریانس Analysis of variancePositron emission tomography - توموگرافی گسیل پوزیترونmessenger ribonucleic acid - رسوب ریبونوکلئیک اسیدPaired helical filament - رشته مارپیچ دوار شدهLipoic acid - لیپوئیک اسیدNIH, National Institutes of Health - مؤسسه ملی سلامتnicotinamide adenine dinucleotide phosphate - نیکوتین آمید adenine dinucleotide phosphateheme oxygenase 1 - همای اکسیژناز 1PET - پتControl - کنترل
موضوعات مرتبط
علوم پزشکی و سلامت
پزشکی و دندانپزشکی
پزشکی و دندانپزشکی (عمومی)
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
A total of 1.7 million traumatic brain injuries (TBIs) occur each year in the United States, but available pharmacologic options for the treatment of acute neurotrauma are limited. Oxidative stress is an important secondary mechanism of injury that can lead to neuronal apoptosis and subsequent behavioral changes. Using a clinically relevant and validated rodent blast model, we investigated how nicotinamide adenine dinucleotide phosphate oxidase (Nox) expression and associated oxidative stress contribute to cellular apoptosis after single and repeat blast injuries. Nox4 forms a complex with p22phox after injury, forming free radicals at neuronal membranes. Using immunohistochemical-staining methods, we found a visible increase in Nox4 after single blast injury in Sprague Dawley rats. Interestingly, Nox4 was also increased in postmortem human samples obtained from athletes diagnosed with chronic traumatic encephalopathy. Nox4 activity correlated with an increase in superoxide formation. Alpha-lipoic acid, an oxidative stress inhibitor, prevented the development of superoxide acutely and increased antiapoptotic markers B-cell lymphoma 2 (t = 3.079, P < 0.05) and heme oxygenase 1 (t = 8.169, P < 0.001) after single blast. Subacutely, alpha-lipoic acid treatment reduced proapoptotic markers Bax (t = 4.483, P < 0.05), caspase 12 (t = 6.157, P < 0.001), and caspase 3 (t = 4.573, P < 0.01) after repetitive blast, and reduced tau hyperphosphorylation indicated by decreased CP-13 and paired helical filament staining. Alpha-lipoic acid ameliorated impulsive-like behavior 7 days after repetitive blast injury (t = 3.573, P < 0.05) compared with blast exposed animals without treatment. TBI can cause debilitating symptoms and psychiatric disorders. Oxidative stress is an ideal target for neuropharmacologic intervention, and alpha-lipoic acid warrants further investigation as a therapeutic for prevention of chronic neurodegeneration.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Translational Research - Volume 166, Issue 6, December 2015, Pages 509-528.e1
Journal: Translational Research - Volume 166, Issue 6, December 2015, Pages 509-528.e1
نویسندگان
Brandon P. Lucke-Wold, Zachary J. Naser, Aric F. Logsdon, Ryan C. Turner, Kelly E. Smith, Matthew J. Robson, Julian E. Bailes, John M. Lee, Charles L. Rosen, Jason D. Huber,