کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10738956 | 1046849 | 2005 | 12 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
A transient treatment of hippocampal neurons with α-tocopherol induces a long-lasting protection against oxidative damage via a genomic action
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کلمات کلیدی
BSOepigallocatechin-gallateMBBRN-acetyl-l-cysteineEGCGNACGSHFCSGFAPNMDAN-methyl-d-aspartateCHXBHTTBHQtert-butylhydroperoxidetert-butylhydroquinoneSDSL-buthionine sulfoximinePBSα-TOHtBuOOHMTT - MTTROS - ROSα-Tocopherol - α-توکوفرولAntioxidant - آنتی اکسیدانIron(II) - آهن (II)Trolox - ترولکسOxidative stress - تنش اکسیداتیوFree radicals - رادیکال آزادsodium dodecyl sulfate - سدیم دودسیل سولفاتfetal calf serum - سرم گوساله جنینcycloheximide - سیکلوهایسیمیدTAP - ضربه زدنantioxidant-responsive element - عنصر پاسخ دهنده آنتی اکسیدانantioxidant responsive element - عنصر پاسخ دهنده آنتی اکسیدانNeuronal culture - فرهنگ نورونیPhosphate-buffered saline - محلول نمک فسفات با خاصیت بافریRat - موش صحراییMonobromobimane - مونوبرموبیمنARE - هستندbutylated hydroxytoluene - هیدروکسی تورولین باتلاقیHippocampus - هیپوکامپ Glial fibrillary acidic protein - پروتئین اسیدی فیبریلاسیون گلایالGlutathione - گلوتاتیونReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
پیش نمایش صفحه اول مقاله

چکیده انگلیسی
Neuroprotection exerted by α-tocopherol against oxidative stress was investigated in cultured rat hippocampal neurons. In addition to its direct action as a radical scavenger revealed at concentrations above 10 μM, a transient application of 1 μM α-tocopherol phosphate (α-TP) to neurons induced a complete delayed long-lasting protection against oxidative insult elicited by exposure to Fe2+ ions, but not against excitotoxicity. A minimal 16-h application of α-TP was required to observe the protection against subsequent oxidative stress. This delayed protection could last up to a week after the application of α-TP, even when medium was changed after the α-TP treatment. Cycloheximide, added either 2 h before or together with α-TP, prevented the delayed neuroprotection, but not the acute. However, cycloheximide applied after the 16-h α-TP pretreatment did not alter the delayed neuroprotection. Neither Trolox, a cell-permeant analogue of α-tocopherol, nor other antioxidants, such as epigallocatechin-gallate and N-acetyl-l-cysteine, elicited a similar long-lasting protection. Only tert-butylhydroquinone could mimic the α-TP effect. Depletion of glutathione (GSH) by l-buthionine sulfoximine did not affect the delayed α-TP protection. Thus, in addition to its acute anti-radical action, α-TP induces a long-lasting protection of neurons against oxidative damage, via a genomic action on antioxidant defenses apparently unrelated to GSH biosynthesis.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Free Radical Biology and Medicine - Volume 39, Issue 8, 15 October 2005, Pages 1009-1020
Journal: Free Radical Biology and Medicine - Volume 39, Issue 8, 15 October 2005, Pages 1009-1020
نویسندگان
Marie Céleste de Jesus Ferreira, Nadine Crouzin, Gérard Barbanel, Catherine Cohen-Solal, Max Récasens, Michel Vignes, Janique Guiramand,