کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6272167 | 1614775 | 2015 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Sulforaphane rescues memory dysfunction and synaptic and mitochondrial alterations induced by brain iron accumulation
ترجمه فارسی عنوان
سولفورفان صرفه جویی در حافظه و تغییرات سیناپسی و میتوکندری ناشی از انباشت آهن مغز
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کلمات کلیدی
HDACopa1 - grandpa1ROS - ROSIron - آهنEDTA - اتیلن دی آمین تترا استیک اسید Ethylenediaminetetraacetic acid - اتیلینیدامین تتراستیک اسیدNeurodegenerative disorders - اختلالات نوروژنیکAlzheimer’s disease - بیماری آلزایمرHuntington’s disease - بیماری هانتینگتونParkinson’s disease - بیماری پارکینسونanalysis of variance - تحلیل واریانسANOVA - تحلیل واریانس Analysis of varianceRecognition memory - حافظه تشخیص یا شناختSulforaphane - سولفورافانMitochondria - میتوکندریاSynapse - همایه یا سیناپسhistone deacetylase - هیستون داستیلازReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
چکیده انگلیسی
Iron overload contributes to the development of neurodegeneration and the exacerbation of normal apoptosis rates, largely due to its participation in the Fenton reaction and production of reactive oxygen species (ROS). Mitochondria constitute the major intracellular source of ROS and the main target of attack by free radicals. They are dynamic organelles that bind (fusion) and divide (fission) in response to environmental stimuli, developmental status, and energy needs of the cells. Sulforaphane (SFN) is a natural compound that displays antioxidant and anti-inflammatory activities. This study aims to investigate the effects of SFN on memory deficits and changes in markers of mitochondrial function, DNM1L and OPA1, and the synaptic marker, synaptophysin, induced by neonatal iron treatment. Male rats received vehicle or carbonyl iron (30Â mg/kg) from the 12th to the 14th postnatal day. In adulthood, they were treated with saline or SFN (0.5 or 5Â mg/kg) for 14Â days every other day. Memory deficits were assessed using the object recognition task. DNM1L, OPA1, and synaptophysin levels in the hippocampus were quantified by Western blotting. Results showed that SFN was able to reverse iron-induced decreases in mitochondrial fission protein, DNM1L, as well as synaptophysin levels in the hippocampus, leading to a recovery of recognition memory impairment induced by iron. These findings suggest that SFN may be further investigated as potential agent for the treatment of cognitive deficits associated with neurodegenerative disorders.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 301, 20 August 2015, Pages 542-552
Journal: Neuroscience - Volume 301, 20 August 2015, Pages 542-552
نویسندگان
I.C. Lavich, B.S. de Freitas, L.W. Kist, L. Falavigna, V.A. Dargél, L.M. Köbe, C. Aguzzoli, B. Piffero, P.Z. Florian, M.R. Bogo, M.N.M. de Lima, N. Schröder,