کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8840783 | 1614697 | 2018 | 27 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Endurance Exercise Mediates Neuroprotection Against MPTP-mediated Parkinson's Disease via Enhanced Neurogenesis, Antioxidant Capacity, and Autophagy
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کلمات کلیدی
DATPeroxiredoxin IIInuclear factor erythroid 2SVZMnSODMPTPCuZnSODHO-1GPXNrf21-methyl-4-phenyl-1,2,3,6-tetrahydropyridine - 1-methyl-4-phenyl-1،2،3،6-tetrahydropyridine5-bromo-2′-deoxyuridine - 5-bromo-2'-deoxyuridineROS - ROSSNpc - SNPCAntioxidant - آنتی اکسیدانAutophagy - اتوفاژیDopamine transporter - انتقال دهنده دوپامینBrdU - بروموداکسی اوریدینParkinson’s disease - بیماری پارکینسونParkinson's disease - بیماری پارکینسونOxidative stress - تنش اکسیداتیوsubstantia nigra pars compacta - توده سیاه پارس متراکمtyrosine hydroxylase - تیروزین هیدروکسیلازmanganese superoxide dismutase - سوپر اکسید دیسموتاز منگنزcopper zinc superoxide dismutase - سوکسوید دیسموتاز روی مسdentate gyrus - شکنج دندانه دارsubventricular zone - منطقه فرعیNeurogenesis - نوروژنزEndurance exercise - ورزش استقامتیglutathione peroxidase - گلوتاتیون پراکسیدازReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
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چکیده انگلیسی
Parkinson's disease (PD) is a neurodegenerative disorder caused by loss of dopaminergic neurons in the substantia nigra, leading to motor dysfunction. Growing evidence has demonstrated that endurance exercise (EE) confers neuroprotection against PD. However, the exact molecular mechanisms responsible for exercise-induced protection of dopaminergic neurons in PD remain unclear. Since oxidative stress plays a key role in the degenerative process of PD. We investigated whether EE-induced neuroprotection is associated with enhanced antioxidative capacity and autophagy, using a mouse model of PD induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) administration. C57BL/6 male mice were randomly assigned to four groups: control (CON, nâ¯=â¯12), exercise (EXE, nâ¯=â¯12), MPTP (MPTP, nâ¯=â¯12) and MPTPâ¯+â¯exercise (MPTPâ¯+â¯EXE, nâ¯=â¯12). Our data demonstrated that while MPTP treatment impaired motor function, EE restored MPTP-induced motor deficits. Our biochemical data showed that EE-induced neuroprotection occurs in combination with multiple synergic neuroprotective pathways: (1) increased neurogenesis shown by an increase in BrdU-positive neurons; (2) diminished loss of dopaminergic neurons evidenced by upregulated tyrosine hydroxylase (TH) and dopamine transporter (DAT) levels; (3) increased antioxidant capacity (e.g., CuZnSOD, CATALASE, GPX1/2, HO-1, DJ1 and PRXIII); and (4) enhanced autophagy (LC3 II, p62, BECLIN1, BNIP3, LAMP2, CATHEPSIN L and TFEB). Our study suggests that EE-induced multiple synergic protective pathways including enhanced neurogenesis, antioxidative capacity, and concordant autophagy promotion contribute to restoration of impaired dopaminergic neuronal function caused by PD. Thus, PD patients should be encouraged to actively participate in regular EE as a potent nonpharmacological therapeutic strategy against PD.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 379, 21 May 2018, Pages 292-301
Journal: Neuroscience - Volume 379, 21 May 2018, Pages 292-301
نویسندگان
Yongchul Jang, Insu Kwon, Wankeun Song, Ludmila M. Cosio-Lima, Youngil Lee,