کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
4341706 | 1295844 | 2007 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Role of reactive oxygen species in modulation of Nrf2 following ischemic reperfusion injury
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کلمات کلیدی
PMSFNrf2−/−t-BHQtert-butylhydroquinoneN-methyl-d-aspartic acidMCAONMDACBFTTCCCANrf2MCADTTECA2,3,5-triphenyltetrazolium chloride - 2،3،5-trihenyltetrazolium chloride3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide - 3- (4،5-dimethylthiazol-2-yl) -2،5-difenyltetrazolium bromideMTT - MTTROS - ROSt-BuOOH - T-BuOOHmiddle cerebral artery occlusion - انسداد شریان (سرخرگ) مغزی میانیcerebral blood flow - جریان خون مغزیdithiothreitol - دیتیوتریتولFree radicals - رادیکال آزادStroke - سکته مغزیmiddle cerebral artery - شریان مغزی میانیexternal carotid artery - شریان کاروتید خارجیcommon carotid artery - شریان کاروتید مشترکTranscription factor - عامل رونویسیantioxidant response element - عنصر پاسخ آنتی اکسیدانnuclear factor erythroid 2-related factor 2 - فاکتور هسته ای عامل erythroid 2 مرتبط 2phenylmethylsulfonyl fluoride - فنیل متیل سولفونیل فلورایدwildtype - نوع وحشیARE - هستندtert-butyl hydroperoxide - هیدروپراکسید تری بوتیلReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله

چکیده انگلیسی
The transcriptional factor Nrf2 has a unique role in various physiological stress conditions, but its contribution to ischemia/reperfusion injury has not been fully explored. Therefore, wildtype (WT) and Nrf2 knockout (Nrf2â/â) mice were subjected to 90-min occlusion of the middle cerebral artery (MCA) followed by 24-h reperfusion to elucidate Nrf2 contribution in protecting against ischemia/reperfusion injury. Infarct volume, represented as percent of hemispheric volume, was significantly (P<0.05) larger in Nrf2â/â mice than in WT mice (30.8±6.1 vs. 17.0±5.1%). Furthermore, neurological deficit was significantly greater in the Nrf2â/â mice. To examine whether neuronal protection was mediated by Nrf2, neurons were treated with various compounds to induce excitotoxic or oxidative stress. Translocation of Nrf2 into the nucleus was increased by the free-radical donor tert-butylhydroperoxide, but not by glutamate or N-methyl-d-aspartic acid (NMDA). In addition, a common Nrf2 inducer, tert-butylhydroquinone, significantly attenuated neuronal cell death induced by tert-butylhydroperoxide (83.6±1.6 vs. 62.0±7.7%) but not as substantially when excitotoxicity was induced by NMDA (91.9±1.6 vs. 79.3±3.3%) or glutamate (87.8±1.5 vs. 80.2±2.6%). The results suggest that Nrf2 reduces ischemic brain injury by protecting against oxidative stress.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 147, Issue 1, 15 June 2007, Pages 53-59
Journal: Neuroscience - Volume 147, Issue 1, 15 June 2007, Pages 53-59
نویسندگان
Z.A. Shah, R.-C. Li, R.K. Thimmulappa, T.W. Kensler, M. Yamamoto, S. Biswal, S. Doré,