کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6271728 | 1614761 | 2016 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Elevation of cortical C26:0 due to the decline of peroxisomal β-oxidation potentiates amyloid β generation and spatial memory deficits via oxidative stress in diabetic rats
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کلمات کلیدی
MDAd-bifunctional proteinEPAβ-secretaseDBPBACE1AβHO-1Eicosapentenoic acidacyl-CoA oxidase 1ACOX1IODNOX4MWMAβPPNADPH oxidase 4 - NADPH اکسیداز 4Docosahexenoic acid - اسید داکوساگزنئیکAlzheimer’s disease - بیماری آلزایمرDHA - دوکوساهگزائنوئیک اسیدDiabetes mellitus - دیابت قندیhigh-fat diet - رژیم غذایی با چربی بالاMorris water maze - ماز آب آب موریسmalondialdehyde - مالون دی آلدهیدheme oxygenase 1 - همای اکسیژناز 1amyloid β precursor protein - پروتئین پیش ماده بتا آمیلوئیدβ-amyloid peptide - پپتید β-آمیلوئید
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Diabetes mellitus correlates with subsequent development of Alzheimer's disease (AD). An accumulation of very long chain fatty acids (VLCFAs) was observed in AD brains. We found previously that inhibiting peroxisomal β-oxidation by an inhibitor caused increases in VLCFA and β-amyloid peptide (Aβ) in the cortex and primary cultured neurons of rats. Therefore, we investigated whether there was an impaired peroxisomal β-oxidation and elevated VLCFA related to the increased Aβ in the diabetic brain. This study was conducted in a type 2 diabetic rat model induced by a high-fat diet and low-dose streptozotocin. A decrease in peroxisomal β-oxidation activity caused by down-regulated thiolase expression and a consequent increase in C26:0 were observed. Meanwhile, decreases in eicosapentenoic acid (EPA) and increases in oxidative stress [indicated by levels of malondialdehyde (MDA), and the protein expression of NOX4, p47phox and HO-1], Aβ, and the expression of AβPP and BACE1, two proteins involved in Aβ production, were observed. C26:0 levels were positively correlated with Aβ and MDA. This work suggests that in addition to decreases in EPA, increases in C26:0 by impaired peroxisomal β-oxidation can be a potential risk factor contributing to the progression of AD in diabetic brains via inducing oxidative stress.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 315, 19 February 2016, Pages 125-135
Journal: Neuroscience - Volume 315, 19 February 2016, Pages 125-135
نویسندگان
Y. Shi, X. Sun, Y. Sun, L. Hou, M. Yao, K. Lian, J. Li, X. Lu, L. Jiang,